Journal articles: 'Prostate Cancer cells Interleukin-6'

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Li, Desheng, Shanbin Zhang, Minfang Zuo, Xinming Hu та Shuming He. "Interleukin-6, Tumor Necrosis Factor-α Expression Levels in Prostate Cancer Tissues and Their Effects on Epithelial Interstitial Transformation, Migration and Invasion in Prostate Cancer Cells". Journal of Biomaterials and Tissue Engineering 10, № 12 (2020): 1773–79. http://dx.doi.org/10.1166/jbt.2020.2496.

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Background: To investigate the expression of Interleukin-6, Interleukin-6 in prostate cancer tissues and its effect on migration and evasiveness of cancer cells. Material and Methods: The releasing of Interleukin-6, Tumor necrosis factor-α in prostate cancer cells was detected by ELISA method. For prostate cancer cells after knockout, additional Interleukin-6 or Tumor necrosis factor-α induction was given in vitro. After 12 h of culture, the effects of Interleukin-6, Tumor necrosis factor-α on the migration and evasiveness of prostate cancer cells were observed by Western blot method and matrices invasion experiment. Results: The expression of epithelial mesenchymal transition-related proteins, the migration and invasion ability of prostate cancer cells in each gene knockout group were significantly reduced. After induction of inflammatory factors (Interleukin-6 or Tumor necrosis factor-α) in the gene knockout group for 12 h, the expression levels of epithelial mesenchymal transition-related proteins, the migration and aggressiveness of prostate cancer were significantly higher than those after knockout. Conclusion: Interleukin-6 and Tumor necrosis factor-α can induce epithelial mesenchymal transition in LNCaP and PC3 cells, promote cell invasion and metastasis, and provide a new direction for future research.

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Chun, Jae Yeon, Nagalakshmi Nadiminty, Smitha Dutt, et al. "Interleukin-6 Regulates Androgen Synthesis in Prostate Cancer Cells." Clinical Cancer Research 15, no. 15 (2009): 4815–22. http://dx.doi.org/10.1158/1078-0432.ccr-09-0640.

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Cross, N. A., M. Papageorgiou, and C. L. Eaton. "Bone marrow stromal cells promote growth and survival of prostate cancer cells." Biochemical Society Transactions 35, no. 4 (2007): 698–700. http://dx.doi.org/10.1042/bst0350698.

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Prostate cancers frequently metastasize to the skeleton, and it has been hypothesized that this environment selectively supports the growth of these tumours. Specifically there is strong evidence that interactions between tumour cells and BMSCs (bone marrow stromal cells) play a major role in supporting prostate cancer growth and survival in bone. Here, we examine factors shown to be secreted by BMSCs, such as IGFs (insulin-like growth factors) and IL-6 (interleukin 6), shown to promote prostate cancer cell proliferation and to potentially replace the requirement for androgens. In addition we discuss another factor produced by BMSCs, osteoprotegerin, which may promote tumour cell survival by suppressing the biological activity of the pro-apoptotic ligand TRAIL (tumour-necrosis-factor-related apoptosis-inducing ligand).

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Afdal, Afdal, Eryati Darwin, Yanwirasti Yanwirasti, and Rizal Hamid. "The Expression of Transforming Growth Factor Beta-1 and Interleukin-6 on Human Prostate: Prostate Hyperplasia and Prostate Cancer." Open Access Macedonian Journal of Medical Sciences 7, no. 12 (2019): 1905–10. http://dx.doi.org/10.3889/oamjms.2019.548.

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BACKGROUND: Prostate hyperplasia and prostate cancer are two of the most common pathological condition of the prostate to be found on male. Both of these diseases share common pathogenesis involving inflammation of prostatic tissues. Chronic inflammation will induce the release of cytokines, followed by cells injury and tissues damage. One of the cytokines that play a role in prostate pathology is IL-6. The inflammation will also induce the releases of anti-inflammatory cytokines such as TGFβ-1.AIM: This study aims to analyse the expression of IL-6 and TGFβ-1, in prostate hyperplasia and prostate cancer. MATERIAL AND METHODS: This is an observational study, using paraffin-embedded tissue samples of prostate hyperplasia and prostate cancer. Samples were obtained from the laboratory of Pathological Anatomy, Faculty of Medicine, Andalas University, Padang, Indonesia. Immunohistochemistry was performed to detect the cytokine expression, and a semiqunatitaves measurement according to Immunoreactive score (IRS) was performed for evaluation. For the TGFβ-1, the stromal expression was also analysed by measurement of the stromal stained area. The correlation of cytokine expression to Gleason index score was also analysed in prostate cancer. RESULTS: The result showed that this study found that TGFβ-1 was detected both in the stromal component as well as epithelial. With the stromal being the dominant site of expression. The stromal TGFβ-1 expression was of significantly higher in prostate hyperplasia compares to prostate cancer (p < 0.05), while the epithelial expression of TGFβ-1 was not found to be significantly different. IL-6 was mostly expressed intracytoplasmic in epithelia. The IL-6 expression was significantly higher in prostate cancer compared to hyperplasia. However, there was no significant correlation to found between IL-6 expression to the Gleason Score among prostate cancers. CONCLUSION: This study concluded that there were differences in expression of both TGFβ-1 and IL-6 between prostate hyperplasia and prostate cancer tissue by immunohistochemistry.

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Feng, Siting, Qizhu Tang, Meng Sun, Jae Yeon Chun, Christopher P. Evans, and Allen C. Gao. "Interleukin-6 increases prostate cancer cells resistance to bicalutamide via TIF2." Molecular Cancer Therapeutics 8, no. 3 (2009): 665–71. http://dx.doi.org/10.1158/1535-7163.mct-08-0823.

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Culig, Zoran, Hannes Steiner, Georg Bartsch, and Alfred Hobisch. "Interleukin-6 regulation of prostate cancer cell growth." Journal of Cellular Biochemistry 95, no. 3 (2005): 497–505. http://dx.doi.org/10.1002/jcb.20477.

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Lin, Yi-Chia, Po-Cheng Liao, Te-Fu Tsai, et al. "Zoledronic Acid Elicits Proinflammatory Cytokine Profile in Osteolytic Prostate Cancer Cells." ISRN Pathology 2014 (April 23, 2014): 1–8. http://dx.doi.org/10.1155/2014/124746.

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Zoledronic acid (ZA), a bisphosphonate used to prevent skeletal fractures in patients with cancers, was demonstrated to induce apoptosis in a number of cancer cells. Our previous study showed that ZA also induces autophagic cell death in metastatic prostate cancer cells. However, the clinical trials using ZA in the treatment of metastatic prostate cancer did not have a longer diseases-free period. Since most of ZA was attracted to the bone after administration, we hypothesized that local prostate cancer cells may evolve prosurvival pathways upon low concentration of ZA treatment. In this study, we investigated the inflammatory effects of ZA on osteolytic PC3 prostate cancer cell, since inflammation was reported to be related to cancer development and survival. Exposure of PC3 cells to various concentrations of ZA resulted in induction of apoptosis and autophagy. The expression of inflammatory biomarkers including interleukin 6 (IL-6), cyclooxygenase-2 (COX-2), and NF-κB was remarkably upregulated in response to ZA treatment in a dose- and time-dependent manner. The production of IL-6 was elevated upon ZA treatment. The antiapoptotic protein Bcl2 was increased with parallel increased level of IL-6. Our data suggest that treatment with low concentrations of ZA enhances the inflammatory profile and may serve as a prosurvival signaling pathway in PC3 cells.

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Deeble, Paul D., Daniel J. Murphy, Sarah J. Parsons, and Michael E. Cox. "Interleukin-6- and Cyclic AMP-Mediated Signaling Potentiates Neuroendocrine Differentiation of LNCaP Prostate Tumor Cells." Molecular and Cellular Biology 21, no. 24 (2001): 8471–82. http://dx.doi.org/10.1128/mcb.21.24.8471-8482.2001.

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ABSTRACT Neuroendocrine (NE) differentiation in prostatic adenocarcinomas has been reported to be an early marker for development of androgen independence. Secretion of mitogenic peptides from nondividing NE cells is thought to contribute to a more aggressive disease by promoting the proliferation of surrounding tumor cells. We undertook studies to determine whether the prostate cancer cell line LNCaP could be induced to acquire NE characteristics by treatment with agents that are found in the complex environment in which progression of prostate cancer towards androgen independence occurs. We found that cotreatment of LNCaP cells with agents that signal through cyclic AMP-dependent protein kinase (PKA), such as epinephrine and forskolin, and with the cytokine interleukin-6 (IL-6) promoted the acquisition of an NE morphological phenotype above that seen with single agents. Convergent IL-6 and PKA signaling also resulted in potentiated mitogen-activated protein kinase (MAPK) activation without affecting the level of signal transducer and activator of transcription or PKA activation observed with these agents alone. Cotreatment with epinephrine and IL-6 synergistically increased c-fos transcription as well as transcription from the β4 nicotinic acetylcholine receptor subunit promoter. Potentiated transcription from these elements was shown to be dependent on the MAPK pathway. Most importantly, cotreatment with PKA activators and IL-6 resulted in increased secretion of mitogenic neuropeptides. These results indicate that PKA and IL-6 signaling participates in gene transcriptional changes that reflect acquisition of an NE phenotype by LNCaP cells and suggest that similar signaling mechanisms, particularly at sites of metastasis, may be responsible for the increased NE content of many advanced prostate carcinomas.

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Tsui, Ke-Hung, Kang-Shuo Chang, Hsin-Ching Sung та ін. "Mucosa-Associated Lymphoid Tissue 1 Is an Oncogene Inducing Cell Proliferation, Invasion, and Tumor Growth via the Upregulation of NF-κB Activity in Human Prostate Carcinoma Cells". Biomedicines 9, № 3 (2021): 250. http://dx.doi.org/10.3390/biomedicines9030250.

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Prostate cancer is one of the most common seen malignancies and the leading cause of cancer-related death among men. Given the importance of early diagnosis and treatment, it is worth to identify a potential novel therapeutic target for prostate cancer. Mucosa-associated lymphoid tissue 1 (MALT1) is a novel gene involved in nuclear factor κB (NF-κB) signal transduction by acting as an adaptor protein and paracaspase, with an essential role in inflammation and tumorigenesis in many cancers. This study investigated the functions and the potential regulatory mechanisms of MALT1 in the human prostate cancer cells. We found that MALT1 is abundant in prostate cancer tissues. MALT1 facilitated NF-κB subunits (p50 and p65) nuclear translocation to induce gene expression of interleukin 6 (IL-6) and C-X-C motif chemokine 5 (CXCL5) in prostate carcinoma cells. MALT1 promoted cell proliferation, invasion, and tumor growth in vitro and in vivo. MALT1 enhanced NF-κB activity in prostate carcinoma cells; moreover, NF-κB induced MALT1 expression determined by reporter and immunoblot assays, implying there is a positive feedback loop between MALT1 and NF-κB. In conclusion, MALT1 is a NF-κB-induced oncogene in the human prostate carcinoma cells.

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Zheng, Xiaoli, and Jin Chu. "Up-regulation of interleukin-33 serum levels in metastatic prostate cancer." American Journal of BioMedicine 4, no. 1 (2016): 56–70. http://dx.doi.org/10.18081/2333-5106/016-56-70.

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Prostate cancer is one of the most frequent cancers worldwide. IL-33 is the most recently described member of the IL-1 family of cytokines and is a ligand for the ST2 receptor. IL-33 is expressed intracellularly predominantly by stromal cells such as endothelial and epithelial cells as well as smooth muscle cells and fibroblasts and it is involved in the pathogenesis of different inflammatory process. The present study was undertaken to evaluate the prognostic significance of the serum levels IL-33 in patients with prostate cancer Ninety-five patients with prostate cancer, ages 59–88 years (71.2 ± 0.34 years), were examined in the present study, the exclusion criteria were presence of autoimmune diseases and none were under any treatment for prostate cancer at the time of examination. The diagnosis of prostate cancer was confirmed by needle biopsy or by C. Blood for the measurement of serum IL-33 was collected into nonheparinized tubes. Prognostic significance of tumor on disease-specific survival was assessed using univariate and multivariate Cox’s proportional hazards model analyses. Serum IL-33 levels were significantly higher in patients with metastatic prostate cancer than in patients with stage B and stage C prostate cancer, and univariate analysis demonstrated that IL-33 was associated with a poor prognosis in metastatic prostate cancer patients. These results indicate that the serum IL-33 level may be associated with the prognosis of patients with prostate cancer.

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Kroon, P., P. A. Berry, D. Bhasin, et al. "301 Interleukin-6 Expression and JAK-STat Signalling in Prostate Cancer Stem Cells." European Journal of Cancer 48 (July 2012): S74. http://dx.doi.org/10.1016/s0959-8049(12)70995-4.

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Pihlstrøm, Nicklas, Yang Jin, Zeynep Nenseth, Omer F. Kuzu, and Fahri Saatcioglu. "STAMP2 Expression Mediated by Cytokines Attenuates Their Growth-Limiting Effects in Prostate Cancer Cells." Cancers 13, no. 7 (2021): 1579. http://dx.doi.org/10.3390/cancers13071579.

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Inflammatory events and dysregulated cytokine expression are implicated in prostate cancer (PCa), but the underlying molecular mechanisms are poorly understood at present. We have previously identified six transmembrane protein of the prostate 2 (STAMP2, also known as STEAP4) as an androgen-regulated gene, as well as a key regulator of PCa growth and survival. STAMP2 is also regulated by, and participates in, inflammatory signaling in other tissues and pathologies. Here, we show that the proinflammatory cytokines interleukin 6 (IL-6) and Interleukin 1 beta (IL-1β) significantly increase and strongly synergize in promoting STAMP2 expression in PCa cells. The two cytokines increase androgen-induced STAMP2 expression, but not expression of other known androgen target genes, suggesting a unique interplay of androgens and cytokines in regulating STAMP2 expression. Interestingly, STAMP2 knockdown significantly increased the ability of IL-6 and IL-1β to inhibit PCa cell growth in vitro. These results suggest that STAMP2 may represent a unique node through which inflammatory events mediate their effects on PCa growth and survival.

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Degeorges, Armelle, Roger Tatoud, Françoise Fauvel-Lafeve, et al. "Stromal cells from human benign prostate hyperplasia produce a growth-inhibitory factor for LNCaP prostate cancer cells, identified as interleukin-6." International Journal of Cancer 68, no. 2 (1996): 207–14. http://dx.doi.org/10.1002/(sici)1097-0215(19961009)68:2<207::aid-ijc12>3.0.co;2-7.

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Gernone, Angela, Senia Trabucco, Leonardo Resta, and Anna Napoli. "Expression of somatostatin receptor subtypes, aurora kinase A, and interleukin-6 in prostate cancer before androgen ablation." Journal of Clinical Oncology 35, no. 6_suppl (2017): e564-e564. http://dx.doi.org/10.1200/jco.2017.35.6_suppl.e564.

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e564 Background: Neuroendocrine differentiation (NED) in prostate cancer (PC) can be detected by immunohistochemistry as single cells in conventional adenocarcinoma. The extent of NED is associated with poor prognosis and early onset of castrate resistant prostate cancer. Aurora kinase A (AURKA) and Interleukin-6 (IL-6) cooperate to induce NED. The aim of this study was to correlate the expression of somatostatin receptor (SSTR) 1- 2- 3- 4- 5 subtypes, AURKA and IL-6 in primary PC with NED pattern and OS. Methods: PC tissues were reviewed from 60 pts who had undergone biopsy or radical prostatectomy for previously untreated advanced or metastatic PC from 2010 to 2016. 10 samples expressed histologically chromogranin A (CgA), a marker of NED expression. Median age was 67 years (47-80), Gleason score ≥ 7, median PSA was 60 ng/ml (1.3-1000), ECOG 0/1 and bone-visceral sites measurable in 90% of cases. For comparison purposes, 8 pathology specimens from pts with primary PC were used. Results: SSTR1-2-4-5 were detected in the nucleus of PC cells in 10/10 samples. SSTR3 and AURKA were not expressed in all 10 samples. IL-6 was detected in 9/10 samples. All 10 pts were associated with a more aggressive clinical course and OS was < 12 mos. Conclusions: In metastatic prostate cancer, pretreatment NED pattern can be a predictor for progression and survival after hormonal and chemotherapy. SSTRs and somatostatin analogs are not potential targets for prostate cancer.

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Al-Bakheit, Ala’a, Saeid Abu-Romman, Ahmad Sharab, and Mohammad Al Shhab. "Anti-inflammatory effect of Varthemia iphionoides extracts against prostate cancer in vitro." European Journal of Inflammation 15, no. 1 (2017): 8–14. http://dx.doi.org/10.1177/1721727x17702151.

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Varthemia iphionoides is a Jordanian medicinal plant with several health-promoting properties, including antibacterial, antioxidant and anticancer activities. However, its anti-inflammatory properties have been poorly investigated up to date. The current study aimed to investigate the anti-inflammatory effect of V. iphionoides by measuring the production of interleukin-6 in response to a pro-inflammatory stimulus (bacterial lipopolysaccharide) in in vitro cell models of human MRC-5 and PC3 cells. We observed a significant reduction in lipopolysaccharide-induced interleukin-6 release in response to V. iphionoides (125 µg/mL) in both non-cancerous fibroblast MRC-5 and prostate cancerous PC3 cells. However, the anti-inflammatory effect of this medicinal plant was stronger when MRC-5 cells were treated with an aqueous extract, while the methanolic extract was more potent in PC3 cells. The effect of V. iphionoides in reducing interleukin-6 production was not due to its cytotoxicity, and future studies are required to elucidate the mechanisms of action by which this medicinal plant modulates inflammatory responses. In conclusion, the results of our study represent the first report of the potential protective effect of water and methanolic extracts of V. iphionoides against pro-inflammatory stimuli in fibroblasts and cancer cells of human origin, and it is critically important to identify the phytochemical compounds responsible for this effect.

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Samiea, Abrar, Jeff S. J. Yoon, Christopher J. Ong, Amina Zoubeidi, Thomas C. Chamberlain, and Alice L. F. Mui. "Interleukin-10 Induces Expression of Neuroendocrine Markers and PDL1 in Prostate Cancer Cells." Prostate Cancer 2020 (July 31, 2020): 1–12. http://dx.doi.org/10.1155/2020/5305306.

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Interleukin-10 (IL10) is best studied for its inhibitory action on immune cells and ability to suppress an antitumour immune response. But IL10 also exerts direct effects on nonimmune cells such as prostate cancer epithelial cells. Elevated serum levels of IL10 observed in prostate and other cancer patients are associated with poor prognosis. After first-line androgen-deprivation therapy, prostate cancer patients are treated with androgen receptor antagonists such as enzalutamide to inhibit androgen-dependent prostate cancer cell growth. However, development of resistance inevitably occurs and this is associated with tumour differentiation to more aggressive forms such as a neuroendocrine phenotype characterized by expression of neuron specific enolase and synaptophysin. We found that treatment of prostate cancer cell lines in vitro with IL10 or enzalutamide induced markers of neuroendocrine differentiation and inhibited androgen receptor reporter activity. Both also upregulated the levels of PDL1, which could promote tumour survival in vivo through its interaction with the immune cell inhibitory receptor PD1 to suppress antitumour immunity. These findings suggest that IL10’s direct action on prostate cancer cells could contribute to prostate cancer progression independent of IL10’s suppression of host immune cells.

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Peshkov, Maxim N., Galina P. Peshkova, and Igor V. Reshetov. "The relationship of obesity and prostate cancer (review)." Obesity and metabolism 17, no. 2 (2020): 147–55. http://dx.doi.org/10.14341/omet10301.

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Obesity is a critical risk factor for prostate cancer (PCa). Adipose tissue plays an important role in tumor development, including growth, invasion, and metastasis. Diet and dietary components affect the progression of prostate cancer; however, the mechanisms underlying these associations remain unclear. Extraprostatic prostate tumor cells form a new microenvironment in the periprostatic adipose tissue, which alters these interactions and promotes tumor progression. Hyperinsulinemia leads to an increase in the level of free or biologically active insulin-like growth factor (IGF-1) due to a decrease in the production of IGF-binding proteins. Hypoandrogenism promotes the development of a more aggressive type of prostate cancer (higher Gleason scores). Adipokines of adipose tissue and cytokines (for example, interleukin-6 (IL-6) and tumor necrosis factor (TNF-), angiogenic factors (for example, vascular endothelial growth factor (VEGF), apelin (AGTRL1) and other factors (for example, leptin and adiponectin) have multiple effects on prostate cancer cells. Tumor cells interact directly or indirectly with adipocytes. Yellow (inactive) bone marrow is adipose tissue with separate islands of reticular tissue. It is located in the medullary canals of the tubular bones and in parts of the cells of the cancellous bone. Bone tissue is the object of the most frequent metastasis in prostate cancer, and with age, the content of fat cells in it increases. Bone marrow adipose tissue interacts with tumor cells, osteoblasts and other stromal cells and participates in the organization of the tumor microenvironment. Adipokines are key molecules in the interaction between tumor cells and adipose tissue, which is carried out through various mechanisms. A better understanding of the role of adipose tissue in the induction and progression of prostate cancer will lead to effective therapeutic strategies for this disease.

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Debes, Jose D., Barbara Comuzzi, Lucy J. Schmidt, Scott M. Dehm, Zoran Culig, and Donald J. Tindall. "p300 Regulates Androgen Receptor–Independent Expression of Prostate-Specific Antigen in Prostate Cancer Cells Treated Chronically with Interleukin-6." Cancer Research 65, no. 13 (2005): 5965–73. http://dx.doi.org/10.1158/0008-5472.can-04-2837.

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Burbridge, Sophie, Robert Michael Goldstein, Declan Cahill, Simon Chowdhury, and John Maher. "Role of lymphotoxin-a and interleukin-17A in human prostate cancer." Journal of Clinical Oncology 30, no. 5_suppl (2012): 212. http://dx.doi.org/10.1200/jco.2012.30.5_suppl.212.

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212 Background: Infiltrating immune cells have been implicated in prostate carcinogenesis. Murine studies suggest that B-cell-derived lymphotoxin (LT)a may be a key effector in the evolution to castrate-resistant prostate cancer (CRPC) (Ammirante et al, Nature 2011). Lymphotoxin a has also been implicated in the progression of murine fibrosarcoma, where it complements interleukin (IL)-17A, to synergistically enhance NFkB signaling. This interaction may also apply to human prostate cancer since IL-17-producing Th17 cells are abundant in these tumors. However, the role of LTα in human as distinct from murine prostate cancer remains unclear. Clinical validation is vital since murine models poorly recapitulate the behavior of prostate cancer in man. Methods: Serum levels of LTα and IL-17A were measured by ELISA in patients with benign (n=22) and malignant prostate disease (n=87). Samples were from 29 early prostate cancer patients (amenable to radical therapy), 28 with androgen-sensitive (AS) disease and 30 with CRPC. Data were not normally distributed and thus were analyzed by Mann-Whitney U test. Results: Serum LTαand IL-17A were significantly elevated in patients with both CRPC and early stage prostate cancer, compared to those with benign disease. LTαwas significantly raised in CRPC compared to AS disease. IL-17A was significantly higher in the early stage disease compared to AS prostate cancer. Conclusions: Based upon these data, we hypothesize that B-cell derived LTα synergises with Th17 derived IL-17A from the earliest stage of primary tumor development. In support of this, blockade of LTα in prostate cancer-prone (TRAMP) mice delays primary tumor onset and inhibits metastasis. Furthermore, NSAIDs protect more strongly against lifetime risk of prostate cancer in those individuals with an LTα over-producer polymorphism. Prostate cancer preferentially metastasizes to local lymph nodes and bone – sites at which mature B-cells are plentiful. Consequently, tumor-trophic effects of LTα would become increasingly efficient with disease progression. Our data are incompatible with and thus refute the clinical relevance of a role for androgen ablation in promoting LTα-driven CRPC.

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Sakellariou, Christina, Oussama Elhage, Efthymia Papaevangelou, et al. "Prostate cancer cells enhance interleukin-15-mediated expansion of NK cells." BJU International 125, no. 1 (2019): 89–102. http://dx.doi.org/10.1111/bju.14893.

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Chang, Tsui, Lin, Hou, Feng, and Juang. "Migration and Invasion Enhancer 1 Is an NF-ĸB-Inducing Gene Enhancing the Cell Proliferation and Invasion Ability of Human Prostate Carcinoma Cells In Vitro and In Vivo." Cancers 11, no. 10 (2019): 1486. http://dx.doi.org/10.3390/cancers11101486.

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: Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed. We determined the expression, biological functions, and regulatory mechanisms of MIEN1 in the prostate. The results of immunohistochemical analysis indicated that MIEN1 was expressed specifically in epithelial cells and significantly higher in adenocarcinoma as compared to in normal tissues. MIEN1 enhanced in vitro cell proliferation, invasion, and in vivo tumorigenesis. Meanwhile, MIEN1 attenuated cisplatin-induced apoptosis in PC-3 cells. Overexpression of NF-ĸB-inducing kinase (NIK) enhanced MIEN1 expression, while overexpression of NF-ĸB inhibitor α (IĸBα) blocked MIEN1 expression in PC-3 cells. In prostate carcinoma cells, MIEN1 provoked Akt phosphorylation; moreover, MIEN1 downregulated N-myc downstream regulated 1 (NDRG1) but upregulated interleukin-6 (IL-6) gene expression. MK2206, an Akt inhibitor, impeded the modulation of MIEN1 on NDRG1 and IL-6 expressions. Our studies suggest that MIEN1 is an NF-ĸB downstream oncogene in the human prostate. Accordingly, the modulation of Akt signaling in the gene expressions of NDRG1 and IL-6 may account for the functions of MIEN1 in cell proliferation, invasion, and tumorigenesis in prostate carcinoma cells.

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Steiner, Hannes, Ilaria T. Cavarretta, Patrizia L. Moser, et al. "Regulation of growth of prostate cancer cells selected in the presence of interleukin-6 by the anti-interleukin-6 antibody CNTO 328." Prostate 66, no. 16 (2006): 1744–52. http://dx.doi.org/10.1002/pros.20492.

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Tsui, Ke-Hung, Ying-Ling Chang, Tsui-Hsia Feng, et al. "Growth differentiation factor-15 upregulates interleukin-6 to promote tumorigenesis of prostate carcinoma PC-3 cells." Journal of Molecular Endocrinology 49, no. 2 (2012): 153–63. http://dx.doi.org/10.1530/jme-11-0149.

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Growth differentiation factor-15 (GDF15), a member of the transforming growth factor-β superfamily, is associated with human cancer progress. We evaluated the role GDF15 plays in tumorigenesis of prostate carcinoma PC-3 cells. Results from real-time RT-PCR and ELISA revealed that expression of GDF15 was approximately threefold higher in LNCaP cells than in PC-3 cells. Other prostate cell lines (PZ-HPV-7, CA-HPV-10, and DU145 cells) expressed extremely low levels of GDF15. Stable overexpression of GDF15 in PC-3 cells enhanced the degree of cell proliferation and invasion as shown in the 3H-thymidine incorporation assay and in the Matrigel invasion assay respectively. Soft agar assays and xenograft animal studies indicated that overexpression of GDF15 in PC-3 cells increased tumorigenesis in vitro and in vivo. Results from RT-PCR, immunoblot, and reporter assays revealed that overexpression of GDF15 resulted in decreased expression of maspin and upregulation of interleukin-6 (IL6), matriptase, and N-myc downstream-regulated gene 1 (NDRG1) expression. Further studies revealed that overexpression of IL6 enhanced GDF15 expression in LNCaP cells while knockdown of IL6 blocked the expression of GDF15 in PC-3 cells, suggesting that expression of GDF15 is upregulated by IL6. This study demonstrated that expression of GDF15 induces cell proliferation, invasion, and tumorigenesis of prostate carcinoma PC-3 cells. The enhancement of tumorigenesis and invasiveness of prostate carcinoma cells that stably overexpress GDF15 may be caused by the dysregulation of maspin, matriptase, and IL6 gene expression. The expression of GDF15 and IL6 is controlled via a positive feedback loop in PC-3 cells.

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Fan, Yu-Ching, Kuan-Der Lee, and Yuan-Chin Tsai. "Roles of Interleukin-1 Receptor Antagonist in Prostate Cancer Progression." Biomedicines 8, no. 12 (2020): 602. http://dx.doi.org/10.3390/biomedicines8120602.

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Background: Inflammation is known to promote tumor formation and progression; however, we found a natural anti-inflammatory factor, interleukin (IL)-1 receptor antagonist (IL1RN), in a mouse transgenic adenocarcinoma of the mouse prostate (TRAMP)-C1-derived tumor microenvironment (TME). We sought to characterize the functions of the IL1RN-secreting cells in the TME. Methods: We compared tumors collected from two syngeneic mouse models and isolated tumor-infiltrating leukocytes (TILs) with different cluster of differentiation 11b (CD11b) statuses. We examined the proliferation functions of the TILs and the IL1RN using several approaches, including a colony-formation assay and DNA synthesis levels. Results: We demonstrated that CD11b-deficient TILs (TILs/CD11b−) secreted the IL1RN and promoted proliferation by analyzing conditioned media. In addition to mouse TRAMP-C1, proliferation functions of the IL1RN were confirmed in several human castration-resistant prostate cancer (CRPC) cell lines and one normal epithelial cell line. The androgen-sensitive lymph node carcinoma of the prostate (LNCaP) cell line showed cytotoxic responses to IL1β treatment and androgen-dependent regulation of IL-1 receptor type 1 (IL1R1), while the C4-2 CRPC cell line did not. IL1RN rescued LNCaP cells from the cytotoxic effects of IL1β/IL1R1 signaling. Conclusions: Our results support TILs/CD11b− cells being able to protect androgen-dependent cells from inflammatory damage and promote the malignant progression of prostate cancers partly through the IL1RN in the TME.

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Puhr, Martin, Frédéric R. Santer, Hannes Neuwirt, Gemma Marcias, Alfred Hobisch, and Zoran Culig. "SOCS-3 antagonises the proliferative and migratory effects of fibroblast growth factor-2 in prostate cancer by inhibition of p44/p42 MAPK signalling." Endocrine-Related Cancer 17, no. 2 (2010): 525–38. http://dx.doi.org/10.1677/erc-10-0007.

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Fibroblast growth factor-2 (FGF-2) is highly expressed in prostate cancer. It promotes tumour progression through multiple pathways including those of signal transducers and activators of transcription factor 3 (STAT3), mitogen-activated protein kinases (MAPKs) and Akt. In previous studies, we have reported that STAT3 phosphorylation inversely correlates with suppressor of cytokine signalling-3 (SOCS-3) expression in prostate cancer cells. Recently, it has become evident that SOCS-3-negative regulation is not only limited to the interleukin-6 (IL-6) receptor. We hypothesised that SOCS-3 interferes with FGF signalling, thus influencing the outcome of its action in prostate cancer cells. For this purpose, we treated DU-145 and LNCaP-IL-6+ cells with increasing concentrations of FGF-2, and verified protein phosphorylation. In the presence of FGF-2, neither STAT3, STAT1, nor Akt could be phosphorylated. Solely the p44/p42 MAPK pathway was activated after FGF-2 stimulation. We show for the first time that SOCS-3 interferes with the FGF-2 signalling pathway by modulating p44 and p42 phosphorylation in prostate cancer cells. Decreased SOCS-3 protein expression results in increased MAPK phosphorylation, whereas SOCS-3 overexpression leads to a decreased cellular proliferation and migration. On the basis of the present results, we propose that SOCS-3 is a novel modulator of FGF-2-regulated cellular events in prostate cancer.

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Omokehinde, Tolu, and Rachelle W. Johnson. "GP130 Cytokines in Breast Cancer and Bone." Cancers 12, no. 2 (2020): 326. http://dx.doi.org/10.3390/cancers12020326.

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Breast cancer cells have a high predilection for skeletal homing, where they may either induce osteolytic bone destruction or enter a latency period in which they remain quiescent. Breast cancer cells produce and encounter autocrine and paracrine cytokine signals in the bone microenvironment, which can influence their behavior in multiple ways. For example, these signals can promote the survival and dormancy of bone-disseminated cancer cells or stimulate proliferation. The interleukin-6 (IL-6) cytokine family, defined by its use of the glycoprotein 130 (gp130) co-receptor, includes interleukin-11 (IL-11), leukemia inhibitory factor (LIF), oncostatin M (OSM), ciliary neurotrophic factor (CNTF), and cardiotrophin-1 (CT-1), among others. These cytokines are known to have overlapping pleiotropic functions in different cell types and are important for cross-talk between bone-resident cells. IL-6 cytokines have also been implicated in the progression and metastasis of breast, prostate, lung, and cervical cancer, highlighting the importance of these cytokines in the tumor–bone microenvironment. This review will describe the role of these cytokines in skeletal remodeling and cancer progression both within and outside of the bone microenvironment.

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Laera, Luna, Nicoletta Guaragnella, Sergio Giannattasio, and Loredana Moro. "6-Thioguanine and Its Analogs Promote Apoptosis of Castration-Resistant Prostate Cancer Cells in a BRCA2-Dependent Manner." Cancers 11, no. 7 (2019): 945. http://dx.doi.org/10.3390/cancers11070945.

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Background: Mutations in the oncosuppressor gene BReast CAncer susceptibility gene 2 (BRCA2) predispose to aggressive forms of prostate cancer which show poor response to taxane-based therapy, the standard treatment for castration-resistant, aggressive prostate cancer. Herein, we addressed the question whether changes in BRCA2 expression, a potential surrogate marker for BRCA2 activity, may affect the response of castration-resistant prostate cancer cells to 6-thioguanine (6-TG), a thiopurine used in the treatment of haematological malignancies. Methods: Yeast, normal prostate cells and castration-resistant prostate cancer cells were treated with 6-TG or its analogues, in presence or absence of paclitaxel, or with olaparib, a poly-(ADP-ribose) polymerase (PARP) inhibitor currently in clinical trials for treatment of metastatic castration-resistant prostate cancer, and cell proliferation, apoptosis and androgen receptor (AR) levels were measured. Results: 6-TG inhibited cell proliferation in yeast, normal and castration-resistant prostate cancer cells but promoted apoptosis only in cancer cells. Suppression of BRCA2 expression by siRNA or shRNA increased the sensitivity to 6-TG- and olaparib-induced apoptosis but did not affect cancer cell response to taxane. Intriguingly, 6-TG reduced AR expression levels independently on BRCA2 expression. Instead, olaparib decreased AR levels only in BRCA2-knockdown prostate cancer cells. Notably, overexpression of BRCA2 resulted in resistance of castration-resistant prostate cancer cells to 6-TG-, taxane- and olaparib-based treatment but promoted sensitivity to apoptosis induced by 2-amino-6-bromopurine and 2,6–dithiopurine, two 6-TG analogues. Conclusions: Our results provide a pre-clinical rationale for the use of 6-TG in the treatment of BRCA2-deficient castration-resistant prostate cancers, and of certain 6-TG analogues for treatment of BRCA2-proficient prostate cancers.

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Chung, T. D., J. J. Yu, M. T. Spiotto, and T. A. Kong. "Phosphatidylinositol-3 kinase is activated by interleukin-6 and inhibits apoptosis in human prostate cancer cells." International Journal of Radiation Oncology*Biology*Physics 48, no. 3 (2000): 247. http://dx.doi.org/10.1016/s0360-3016(00)80291-6.

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Kwon, Gyoo Taik, Jae In Jung, Hye Rim Song, et al. "Piceatannol inhibits migration and invasion of prostate cancer cells: possible mediation by decreased interleukin-6 signaling." Journal of Nutritional Biochemistry 23, no. 3 (2012): 228–38. http://dx.doi.org/10.1016/j.jnutbio.2010.11.019.

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Tassidis, Helena, Zoran Culig, Anette Gjörloff Wingren, and Pirkko Härkönen. "Role of the protein tyrosine phosphatase SHP-1 in Interleukin-6 regulation of prostate cancer cells." Prostate 70, no. 14 (2010): 1491–500. http://dx.doi.org/10.1002/pros.21184.

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Sivashanmugam, Perumal, Linda Tang, and Yehia Daaka. "Interleukin 6 Mediates the Lysophosphatidic Acid-regulated Cross-talk between Stromal and Epithelial Prostate Cancer Cells." Journal of Biological Chemistry 279, no. 20 (2004): 21154–59. http://dx.doi.org/10.1074/jbc.m313776200.

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Weaver, Erika M., Francis J. Zamora, Jennifer L. Hearne, and Miguel Martin-Caraballo. "Posttranscriptional regulation of T-type Ca 2+ channel expression by interleukin-6 in prostate cancer cells." Cytokine 76, no. 2 (2015): 309–20. http://dx.doi.org/10.1016/j.cyto.2015.07.004.

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Natani, Sirisha, Vishnu M. Dhople, Asha Parveen, et al. "AMPK/SIRT1 signaling through p38MAPK mediates Interleukin-6 induced neuroendocrine differentiation of LNCaP prostate cancer cells." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1868, no. 10 (2021): 119085. http://dx.doi.org/10.1016/j.bbamcr.2021.119085.

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Yu, Xiaoqin, Ran Chen, Fei Wang, et al. "Pattern recognition receptor-initiated innate immune responses in mouse prostatic epithelial cells." Biology of Reproduction 105, no. 1 (2021): 113–27. http://dx.doi.org/10.1093/biolre/ioab076.

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Abstract Three major pathogenic states of the prostate, including benign prostatic hyperplasia, prostate cancer, and prostatitis, are related to the local inflammation. However, the mechanisms underlying the initiation of prostate inflammation remain largely unknown. Given that the innate immune responses of the tissue-specific cells to microbial infection or autoantigens contribute to local inflammation, this study focused on pattern recognition receptor (PRR)-initiated innate immune responses in mouse prostatic epithelial cells (PECs). Primary mouse PECs abundantly expressed Toll-like receptor 3 (TLR3), TLR4, TLR5, melanoma differentiation-associated protein 5 (MDA5), and IFN-inducible protein 16 (p204 in mouse). These PRRs can be activated by their respective ligands: lipopolysaccharide (LPS) and flagellin of Gram-negative bacteria for TLR4 and TLR5, polyinosinic-polycytidylic acid (poly(I:C)) for TLR3 and MDA5, and herpes simplex virus DNA analog (HSV60) for p204. LPS and flagellin predominantly induced the expression of inflammatory cytokines, including tumor necrosis factor alpha (TNFA), interleukin 6 (IL6), chemokines monocyte chemoattractant protein-1 (MCP1), and C-X-C motif chemokine 10 (CXCL10). Poly(I:C) and HSV60 predominantly induced the expression of type 1 interferons (IFNA and IFNB) and antiviral proteins: Mx GTPase 1, 2′,5′-oligoadenylate synthetase 1, and IFN-stimulated gene 15. The replication of mumps virus in PECs was inhibited by type 1 IFN signaling. These findings provide insights into the mechanisms underlying innate immune response in the prostate.

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Santer, Frédéric R., Kamilla Malinowska, Zoran Culig, and Ilaria T. Cavarretta. "Interleukin-6 trans-signalling differentially regulates proliferation, migration, adhesion and maspin expression in human prostate cancer cells." Endocrine-Related Cancer 17, no. 1 (2010): 241–53. http://dx.doi.org/10.1677/erc-09-0200.

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Interleukin-6 (IL-6) is suggested to have a pathogenic role in the progression of prostate cancer (PC), therefore representing an attractive target for new therapies. However, due to the pleiotropy of this cytokine, targeting IL-6 results in different and unpredictable responses. In order to better understand the mechanisms underlying the different responses to the cytokine, we focused our attention on IL-6 receptors (IL-6Rs) that represent the first element in the cascade of cytokine-activated signalling pathways. IL-6 signal transduction may indeed occur through the membrane IL-6R (classical signalling) and/or through the less studied soluble IL-6R (sIL-6R; IL-6 trans-signalling (IL-6TS)). We provide the first evidence how responses to IL-6 may depend on the different content of IL-6Rs in PC. In particular, the studies of 3H-thymidine incorporation and exploitation of different approaches (i.e. activation or inhibition of IL-6TS in sIL-6R-negative and -positive cell lines and transfection of IL-6R siRNA) allowed us to demonstrate that IL-6TS specifically accounts for an anti-proliferative effect of the cytokine in three PC cell lines that are known to respond differently to IL-6. Additionally, by applying migration-, scratch- and adhesion assays, we show that IL-6TS increases motility and migration and decreases adhesion of prostate cells facilitating thereby processes that determine metastasis initiation and spread. Finally, by western analyses, we uncovered an IL-6- and sIL-6R-dependent downregulation of the tumour suppressor maspin. Collectively, these data suggest that selective targeting of IL-6TS might allow to refine the currently available experimental anti-IL-6 therapies against PC.

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Galustian, Christine, Annapurna Vyakarnam, Oussama Elhage, Oliver Hickman, Prokar Dasgupta, and Richard A. Smith. "Immunotherapy of prostate cancer: identification of new treatments and targets for therapy, and role of WAP domain-containing proteins." Biochemical Society Transactions 39, no. 5 (2011): 1433–36. http://dx.doi.org/10.1042/bst0391433.

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Prostate adenocarcinoma is present in over 80% of men over the age of 80 and is by far the most common cancer of men. Although radical prostatectomy is curative in early disease, the risks of incontinence and impotence can affect the quality of life of patients. Early intervention with localized immunotherapy represents a potential solution as lymphocyte infiltration does occur in prostate cancer lesions, and immunotherapy with dendritic cell vaccines can significantly increase survival in late stage disease. However, lymphocytic infiltrates in the cancerous prostates have an anergic character arising from the suppressive effects of the microenvironment resulting from a conversion of effector cells into regulatory T-cells. Although TGFβ (transforming growth factor β) and IL-10 (interleukin-10) are known to be strong suppressor molecules associated with prostate cancer, they are among many possible suppressive factors. We discuss the possible role of alternative suppressor molecules, including the WAP (whey acidic protein) homologue ps20 that is expressed on prostate stroma and other WAP domain-containing proteins in the immunosuppressive prostate cancer milieu and discuss novel immunotherapeutic strategies to combat this disease.

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Kim, Jayoung, Rosalyn M. Adam, Keith R. Solomon, and Michael R. Freeman. "Involvement of Cholesterol-Rich Lipid Rafts in Interleukin-6-Induced Neuroendocrine Differentiation of LNCaP Prostate Cancer Cells." Endocrinology 145, no. 2 (2004): 613–19. http://dx.doi.org/10.1210/en.2003-0772.

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Abstract IL-6 is an inflammatory cytokine that has been linked to aggressive prostate cancer (PCa). Previous studies have demonstrated that IL-6 can enhance the differentiation of PCa cells toward a neuroendocrine (NE) phenotype, a possible indicator of hormone-refractory disease. In this report, we present evidence that the mechanism of IL-6-stimulated NE differentiation employs a detergent-resistant (lipid raft) membrane compartment for signal transduction in LNCaP PCa cells. Signal transducer and activator of transcription (STAT)3, a mediator of IL-6 signaling, was rapidly phosphorylated and translocated to the nucleus in LNCaP cells treated with IL-6. Both processes were inhibited by filipin, a cholesterol-binding compound that disrupts plasma membrane lipid rafts. Isolation of Triton X-100-insoluble raft fractions from LNCaP cells by discontinuous sucrose gradient centrifugation demonstrated that the 80-kDa IL-6 receptor localized almost exclusively to the raft compartment. Although STAT3 was located predominantly in the Triton X-100-soluble subcellular fraction in exponentially growing cells, abundant phosphorylated STAT3 was detected in the raft fraction after stimulation with IL-6. Increases in expression of the NE marker, neuron-specific enolase, and neuron-specific enolase promoter activity after IL-6 treatment were reduced after membrane rafts were disrupted by filipin treatment. LNCaP cells expressed the raft-resident proteins flotillin-2 and Giα2, but notably not caveolins, the predominant structural protein present in caveolar membrane rafts in many tissues and tumor cells. These results are the first to define a role for lipid raft membrane microdomains in signal transduction mechanisms capable of promoting the NE phenotype in PCa cells, and they demonstrate that the raft compartment is capable of mediating such signals in the absence of caveolins. Our results also suggest a mechanistic role for membrane cholesterol in cell signaling events relevant to PCa progression.

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Malinowska, Kamilla, Hannes Neuwirt, Ilaria T. Cavarretta, et al. "Interleukin-6 stimulation of growth of prostate cancer in vitro and in vivo through activation of the androgen receptor." Endocrine-Related Cancer 16, no. 1 (2009): 155–69. http://dx.doi.org/10.1677/erc-08-0174.

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It is hypothesized that ligand-independent activation of the androgen receptor is one of the mechanisms implicated in tumour progression. However, supportive evidence is limited to the effect of HER-2/neu that stimulates prostate cancer progression through activation of the androgen receptor. In the present study, we have asked whether the proinflammatory cytokine interleukin-6 (IL-6), which is known to stimulate androgen receptor activity and expression of its downstream target genes, may also induce growth of androgen-sensitive cells. We have found that IL-6 differentially regulates proliferation of LAPC-4 and MDA PCa 2b cells. In MDA PCa 2b cells, growth stimulation by IL-6 was reversed by administration of either the non-steroidal anti-androgen bicalutamide or the inhibitor of the mitogen-activated protein kinase pathway PD98059. Neither cell line was found to express endogenous IL-6. Interestingly, the treatment of those prostate cancer cells did not increase phosphorylation of STAT3. The effect of IL-6 on stimulation of androgen receptor activity in MDA PCa 2b cells was lower than that of androgen, comparable with findings reported by other researchers. However, growth of MDA PCa 2b xenografts in castrated animals treated with IL-6 was similar to that in non-castrated animals. In addition, bicalutamide showed an inhibitory effect on IL-6-regulated growth in vivo. Taken together, data in the present study demonstrate that IL-6 may cause growth of androgen receptor-positive tumours in vitro and in vivo through activation of the androgen receptor.

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Culig, Zoran. "Response to Androgens and Androgen Receptor Antagonists in the Presence of Cytokines in Prostate Cancer." Cancers 13, no. 12 (2021): 2944. http://dx.doi.org/10.3390/cancers13122944.

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Non-steroidal anti-androgens have a major role in the treatment of non-localized prostate cancer. Interleukins are involved in the regulation of many cellular functions in prostate cancer and also modify cellular response to anti-androgens. A specific role of selected IL is presented in this review. IL-8 is a cytokine expressed in prostate cancer tissue and microenvironment and promotes proliferation and androgen receptor-mediated transcription. In contrast, IL-1 displays negative effects on expression of androgen receptor and its target genes. A subgroup of prostate cancers show neuroendocrine differentiation, which may be in part stimulated by androgen ablation. A similar effect was observed after treatment of cells with IL-10. Another cytokine which is implicated in regulation of androgenic response is IL-23, secreted by myeloid cells. Most studies on androgens and IL were carried out with IL-6, which acts through the signal transducer and activator of the transcription (STAT) factor pathway. IL-6 is implicated in resistance to enzalutamide. Activation of the STAT-3 pathway is associated with increased cellular stemness. IL-6 activation of the androgen receptor in some prostate cancers is associated with increased growth in vitro and in vivo. Molecules such as galiellalactone or niclosamide have an inhibitory effect on both androgen receptor and STAT-3 pathways.

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Anisimova, Natalia Yu, Andrey V. Sosnov, Nadezhda E. Ustyuzhanina, Gianfranco Baronzio та Mikhail V. Kiselevsky. "Cytotoxic Activity of Peripheral Blood Mononuclear Leukocytes, Activated by Interleukin-2/β-Cyclodextrin Nanocomposition against Androgen Receptor-Negative Prostate Cancers". ISRN Oncology 2011 (17 серпня 2011): 1–7. http://dx.doi.org/10.5402/2011/405656.

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Nanocomposition comprised of interleukin-2 in suboptimal noneffective concentration and β-cyclodextrin was studied in vitro. This preparation as well as interleukin-2 in optimal concentration was shown to increase natural killer activity to K-562 cells and cytotoxicity of activated peripheral blood mononuclear cells (PBMCs) against PC-3 and DU 145 cells. At the same time β-cyclodextrin or interleukin-2 in equimolar concentrations did not influence the spontaneous killer activity of PBMC. This combination of cyclodextrin + interleukin-2 led to the decrease of interleukin-2 effective concentration by an order. This phenomenon could be explained by cyclodextrins ability to promote the formation of nanoparticles with drugs, which results in enhancing their water solubility and bioavailability. Besides, interleukine-2/β-cyclodextrin nanocomposition as opposed to interleukin-2 alone led to increasing the number of not only lymphocytes, but also macrophages contained in activated PBMC population. Application of low concentration of interleukin-2 allowing for good clinical efficiency may significantly mitigate the side effects of the drug and enable to develop adoption of immunotherapy for patients with androgen-resistant prostate cancer.

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Ishiguro, H., K. Akimoto, Y. Nagashima, et al. "aPKC / promotes growth of prostate cancer cells in an autocrine manner through transcriptional activation of interleukin-6." Proceedings of the National Academy of Sciences 106, no. 38 (2009): 16369–74. http://dx.doi.org/10.1073/pnas.0907044106.

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Ishii, Kenichiro, Takeshi Sasaki, Kazuhiro Iguchi, et al. "Interleukin-6 induces VEGF secretion from prostate cancer cells in a manner independent of androgen receptor activation." Prostate 78, no. 11 (2018): 849–56. http://dx.doi.org/10.1002/pros.23643.

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Gilazieva, Zarema, Gulcin Tezcan, Ekaterina Garanina, et al. "IL-6 As a Potential Cell Released Marker of Prostate Cancer Cell Death." Blood 132, Supplement 1 (2018): 4964. http://dx.doi.org/10.1182/blood-2018-99-116076.

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Abstract Introduction: Interleukin 6 (IL-6) is proinflammatory cytokine which is produced by cell when Nod-like receptors (NLRs) are activated. Increased production of IL-6 was shown to promote tumor growth and metastasis.Therefore, it could be suggested that activation of NLRs could support malignancy. PC-3, prostate tumor derived cells, was shown to produce IL-6; however, little is known about the role of NLRs in regulation of cytokine secretion. Method: PC-3 cells were seeded in 48 well plate cell culture plates and culturd in presence of VX765, Nigericin or Camptothesin. After 24 hours incubation, cell death was determined using Annexin V test. Additionally, IL-6 level was assessed in culture medium using Bio-Plex Pro™ Human Chemokine Panel (Biorad). Data was analyzed using One Way Anova, Post Hoc Tukey test, SPSS 20. Results: Viability of PC3 cells was reduced when treated with Nigericin (37.74±0.33%) and Champtothesin (10.10±0.23%) as compared to untreated cells (P<0.01), while VX765 did not affect cell viability (4.78±0.28 %; P= 0.645). Nigerecin significatly increased IL-6 production in PC3 cells when compared to untreated cells. Interestingly, IL-6 levels in culture medium of PC3 cells treated with nigerecin was significantly higher than that in cells treated with VX765 and campthothesin (p< 0.001). Conclusion: It appears that IL-6 can be produced by PC3 cells upon stmulation of NLRs. Since NLRs activation was associated with reduced cell vitality, we suggest that increased IL-6 level in culture medium could be the result of the cytokine release from dead cells. This study was supported by RFBR Grant #18-34-01000 and Program of Competitive Growth of KFU. Disclosures No relevant conflicts of interest to declare.

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Gernone, Angela, Senia Trabucco, Eliano Cascardi, Leonardo Resta, Franco Silvestris, and Anna Napoli. "Expression of androgen receptor, somatostatin receptor subtypes, aurora kinase A, and interleukin-6 in prostate cancer before androgen ablation." Journal of Clinical Oncology 35, no. 15_suppl (2017): e16508-e16508. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e16508.

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e16508 Background: Neuroendocrine differentiation (NED) in prostate cancer (PC) can be detected by immunohistochemistry as single cells in conventional adenocarcinoma. NEPC is a poor-recognized late presentation of hormone refractory subtype of PC AR-negative. NEPC correlates with poor prognosis, tumor progression during androgen-deprivation therapy and frequent visceral metastases. Aurora kinase A (AURKA) and Interleukin-6 (IL-6) cooperate to induce NED. The aim of this study was to correlate the expression of somatostatin receptor (SSTR) 1- 2- 3- 4- 5 subtypes, AURKA and IL-6 in primary PC with NED pattern before androgen ablation and OS. Methods: PC tissues were reviewed from 60 pts who had undergone biopsy or radical prostatectomy for previously untreated advanced or metastatic PC from 2010 to 2016. 10 samples expressed histologically chromogranin A (CgA), a marker of NED expression. Median age was 67 years (47-80), Gleason score ≥ 7, median PSA was 60 ng/ml (1.3-1000), ECOG 0/1 and bone-visceral sites measurable in 90% of cases. For comparison purposes, 8 pathology specimens from pts with primary PC negative for CgA expression were used. Results: SSTR1-2-4-5 were detected only in the nucleus of PC cells in 10/10 samples. AR was expressed in all 10 samples CgA positive. SSTR3 and AURKA were not expressed in all 10 samples. IL-6 was detected in 9/10 samples. All 10 pts developed early onset of CRPC, more aggressive clinical course with rapid occurrence of visceral metastases and OS was < 12 mos. Conclusions: In metastatic prostate cancer, pretreatment NED pattern can be a predictor for progression and survival after hormonal and during standard chemotherapy. Most likely NEPC become AR negative during disease progression and in response to androgen deprivation therapy. We supposed, according to other data, that the novel potent AR-targeted drugs should be not used in this subset of patients. SSTRs and somatostatin analogs are not potential targets for prostate cancer.

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Lee, Jae-Hee, Dae-Young Lee, Hyo-Jung Lee, et al. "Inhibition of STAT3/PD-L1 and Activation of miR193a-5p Are Critically Involved in Apoptotic Effect of Compound K in Prostate Cancer Cells." Cells 10, no. 8 (2021): 2151. http://dx.doi.org/10.3390/cells10082151.

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Since the signal transducer and activator of transcription 3 (STAT3)/programmed death-ligand 1 (PD-L1) signaling plays an important role in tumor-immune microenvironments, in the present study, the role of STAT3/PD-L1 signaling in the apoptotic mechanism of an active ginseng saponin metabolite compound K (CK) was investigated in human prostate cancer cells. Here, CK exerted significant cytotoxicity without hurting RWPE1 normal prostate epithelial cells, increased sub-G1 and cleavage of Poly ADP-ribose polymerase (PARP) and attenuated the expression of pro-PARP and Pro-cysteine aspartyl-specific protease3 (pro-caspase-3) in LANCap, PC-3 and DU145 cells. Further, CK attenuated the expression of p-STAT3 and PD-L1 in DU145 cells along with disrupted the binding of STAT3 to PD-L1. Furthermore, CK effectively abrogated the expression of p-STAT3 and PD-L1 in interferon-gamma (INF-γ)-stimulated DU145cells. Additionally, CK suppressed the expression of vascular endothelial growth factor (VEGF), transforming growth factor-β (TGF-β), interleukin 6 (IL-6) and interleukin 10 (IL-10) as immune escape-related genes in DU145 cells. Likewise, as STAT3 targets genes, the expression of CyclinD1, c-Myc and B-cell lymphoma-extra-large (Bcl-xL) was attenuated in CK-treated DU145 cells. Notably, CK upregulated the expression of microRNA193a-5p (miR193a-5p) in DU145 cells. Consistently, miR193a-5p mimic suppressed p-STAT3, PD-L1 and pro-PARP, while miR193a-5p inhibitor reversed the ability of CK to attenuate the expression of p-STAT3, PD-L1 and pro-PARP in DU145 cells. Taken together, these findings support evidence that CK induces apoptosis via the activation of miR193a-5p and inhibition of PD-L1 and STAT3 signaling in prostate cancer cells.

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Steiner, H., P. A. Berger, S. Godoy-Tundidor, et al. "358 Vascular endothelial growth factor autocrine loop in prostate cancer cells generated after prolonged treatment with interleukin-6." European Urology Supplements 3, no. 2 (2004): 92. http://dx.doi.org/10.1016/s1569-9056(04)90357-0.

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Terakawa, Tomoaki, Hideaki Miyake, Junya Furukawa, Atsushi Takenaka, and Masato Fujisawa. "ENHANCED SENSITIVITY TO ANDROGEN WITHDRAWAL BY OVEREXPRESSION OF INTERLEUKIN-6 IN HUMAN ANDROGEN-DEPENDENT PROSTATE CANCER LNCAP CELLS." Journal of Urology 181, no. 4S (2009): 480. http://dx.doi.org/10.1016/s0022-5347(09)61359-8.

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Xie, Shaozhen, Hui-Kuan Lin, Jing Ni, et al. "Regulation of interleukin-6-mediated PI3K activation and neuroendocrine differentiation by androgen signaling in prostate cancer LNCaP cells." Prostate 60, no. 1 (2004): 61–67. http://dx.doi.org/10.1002/pros.20048.

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Gazi, Mozammel H., Aiyu Gong, Krishna V. Donkena, and Charles Y. F. Young. "Sodium selenite inhibits interleukin-6-mediated androgen receptor activation in prostate cancer cells via upregulation of c-Jun." Clinica Chimica Acta 380, no. 1-2 (2007): 145–50. http://dx.doi.org/10.1016/j.cca.2007.01.031.

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Figueiredo, Marxa L., Rachel Letteri, Delphine Chan-Seng, Shreya Kumar, Cosette M. Rivera-Cruz, and Todd S. Emrick. "Reengineering Tumor Microenvironment with Sequential Interleukin Delivery." Bioengineering 8, no. 7 (2021): 90. http://dx.doi.org/10.3390/bioengineering8070090.

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Some cytokines can reengineer anti-tumor immunity to modify the tumor micro-environment. Interleukin-27 (IL-27) can partially reduce tumor growth in several animal models, including prostate cancer. We hypothesized that addition of IL-18, which can induce the proliferation of several immune effector cells through inducing IFNγ could synergize with IL-27 to enhance tumor growth control. We describe our findings on the effects of IL-27 gene delivery on prostate cancer cells and how sequential therapy with IL-18 enhanced the efficacy of IL-27. The combination of IL-27 followed by IL-18 (27→18) successfully reduced cancer cell viability, with significant effects in cell culture and in an immunocompetent mouse model. We also examined a novel chimeric cytokine, comprising an IL-27 targeted at the C-terminus with a short peptide, LSLITRL (27pepL). This novel cytokine targets a receptor upregulated in tumor cells (IL-6Rα) via the pepL ligand. Interestingly, when we compared the 27→18 combination with the single 27pepL therapy, we observed a similar efficacy for both. This efficacy was further enhanced when 27pepL was sequenced with IL-18 (27pepL→18). The observed reduction in tumor growth and significantly enriched canonical pathways and upstream regulators, as well as specific immune effector signatures (as determined by bioinformatics analyses in the tumor microenvironment) supported the therapeutic design, whereby IL-27 or 27pepL can be more effective when delivered with IL-18. This cytokine sequencing approach allows flexible incorporation of both gene delivery and recombinant cytokines as tools to augment IL-27’s bioactivity and reengineer efficacy against prostate tumors and may prove applicable in other therapeutic settings.

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Journal articles on the topic 'Prostate Cancer cells Interleukin-6'

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