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Journal articles on the topic 'Metastasis and autophagy'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Xu, Funeng, Xilin Li, Xuehui Huang, Jingmei Pan, Yi Wang, and Shaobing Zhou. "Development of a pH-responsive polymersome inducing endoplasmic reticulum stress and autophagy blockade." Science Advances 6, no. 31 (2020): eabb8725. http://dx.doi.org/10.1126/sciadv.abb8725.

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Autophagy is involved in the occurrence and development of tumors. Here, a pH-responsive polymersome codelivering hydroxychloroquine (HCQ) and tunicamycin (Tuni) drugs is developed to simultaneously induce endoplasmic reticulum (ER) stress and autophagic flux blockade for achieving an antitumor effect and inhibiting tumor metastasis. The pH response of poly(β-amino ester) and HCQ synergistically deacidifies the lysosomes, thereby blocking the fusion of autophagosomes and lysosomes and lastly blocking autophagic flux. The function mechanism of regulating autophagy was systematically investigate

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Sahebi, Reza, Nazanin Akbari, Zeynab Bayat, Mohammad Rashidmayvan, Amin Mansoori, and Maria Beihaghi. "A Summary of Autophagy Mechanisms in Cancer Cells." Research in Biotechnology and Environmental Science 1, no. 1 (2022): 28–35. http://dx.doi.org/10.58803/rbes.2022.1.1.06.

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Autophagy is a well-known vital process in cells and plays a significant role in biological evolution, the immune system, and cell death. It can be effective in fatal disorders, such as nervous system degeneration, autoimmune diseases, and cancer. Autophagy has a dual role; on the one hand, it increases cell survival, and on the other hand, it causes cell death in advanced stages although no agreement has yet been accomplished on the role of autophagy in cellular processes. There is evidence that autophagic signaling regulation is inversely related to oncogenic signaling. Numerous commonly act

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Li, Zhennan, Cheng Lu, Fengliang Wang та ін. "Heat treatment-induced autophagy promotes breast cancer cell invasion and metastasis via TGF-β2-mediated epithelial-mesenchymal transitions". PeerJ 11 (12 січня 2023): e14640. http://dx.doi.org/10.7717/peerj.14640.

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Background Insufficient thermal ablation can accelerate malignant behaviors and metastases in some solid tumors, and epithelial-mesenchymal transition (EMT) and autophagy are involved in tumor metastasis. It has been found that TGF-β2 which belongs to the family of transforming growth factors often associated with cancer cell invasiveness and EMT. However, whether the interactions between autophagy and TGF-β2 induce EMT in breast cancer (BC) cells following insufficient microwave ablation (MWA) remains unclear. Methods BC cells were treated with sublethal heat treatment to simulate insufficien

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Denisenko, Tatiana, Anastasia Pivnyuk, and Boris Zhivotovsky. "p53-Autophagy-Metastasis Link." Cancers 10, no. 5 (2018): 148. http://dx.doi.org/10.3390/cancers10050148.

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Mowers, E. E., M. N. Sharifi, and K. F. Macleod. "Autophagy in cancer metastasis." Oncogene 36, no. 12 (2016): 1619–30. http://dx.doi.org/10.1038/onc.2016.333.

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Zhang, Huilin, and Bingjian Lu. "The Roles of ceRNAs-Mediated Autophagy in Cancer Chemoresistance and Metastasis." Cancers 12, no. 10 (2020): 2926. http://dx.doi.org/10.3390/cancers12102926.

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Chemoresistance and metastasis are the main causes of treatment failure and unfavorable outcome in cancers. There is a pressing need to reveal their mechanisms and to discover novel therapy targets. Autophagy is composed of a cascade of steps controlled by different autophagy-related genes (ATGs). Accumulating evidence suggests that dysregulated autophagy contributes to chemoresistance and metastasis via competing endogenous RNA (ceRNA) networks including lncRNAs and circRNAs. ceRNAs sequester the targeted miRNA expression to indirectly upregulate ATGs expression, and thereof participate in au

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Bhattacharyya, Shalmoli, Renaissa De, and Radhika Srinivasan. "Abstract A031: Combination of hedgehog targeting and autophagy inhibitor potentiate cytotoxicity in 3D spheroids of cervical cancer: A promising therapeutic strategy in metastatic disease." Cancer Research 83, no. 2_Supplement_2 (2023): A031. http://dx.doi.org/10.1158/1538-7445.metastasis22-a031.

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Abstract Cervical cancer is the second most common malignancy in women and a major cause of morbidity and mortality worldwide. Statistics show that present biologic therapy has had little impact on survival in recurrent and metastatic disease. Consequently, there is an urgent need to explore the best treatment options for advanced cervical cancer. Hedgehog (Hh) signaling pathway has been shown to play an important role in metastasis, recurrence and drug resistance of cervical cancer. Therefore, inhibition of hedgehog signaling pathway is emerging as a new strategy for the treatment of advanced

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Radovanovic, Milan, Sasenka Vidicevic, Jelena Tasic, et al. "Role of AMPK/mTOR-independent autophagy in clear cell renal cell carcinoma." Journal of Investigative Medicine 68, no. 8 (2020): 1386–93. http://dx.doi.org/10.1136/jim-2020-001524.

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We examined the status and role of autophagy, a process of lysosomal recycling of cellular material, in clear cell renal cell carcinoma (ccRCC). Paired samples of tumor and adjacent non-malignant tissue were collected from 20 patients with ccRCC after radical nephrectomy. The mRNA levels of apoptosis (BAD, BAX, BCL2, BCLXL, BIM) and autophagy (ATG4, BECN1, GABARAP, p62, UVRAG) regulators were measured by RT-qPCR. The protein levels of autophagosome-associated LC3-II, autophagy receptor p62, apoptotic marker PARP, as well as phosphorylation of autophagy initiator Unc 51-like kinase 1 (ULK1), it

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Kim, Hye Min, and Ja Seung Koo. "The Role of Autophagy in Breast Cancer Metastasis." Biomedicines 11, no. 2 (2023): 618. http://dx.doi.org/10.3390/biomedicines11020618.

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Patient morbidity and mortality is significantly increased in metastatic breast cancer. The metastasis process of breast cancer is very complicated and is delicately controlled by various factors. Autophagy is one of the important regulatory factors affecting metastasis in breast cancer by engaging in cell mobility, metabolic adaptation, tumor dormancy, and cancer stem cells. Here, we discuss the effects of autophagy on metastasis in breast cancer and assess the potential use of autophagy modulators for metastasis treatment.

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Yao, Jiaqi, Chi Ma, Kaixuan Feng, Guang Tan, and Qingping Wen. "Focusing on the Role of Natural Products in Overcoming Cancer Drug Resistance: An Autophagy-Based Perspective." Biomolecules 12, no. 11 (2022): 1565. http://dx.doi.org/10.3390/biom12111565.

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Autophagy is a critical cellular adaptive response in tumor formation. Nutritional deficiency and hypoxia exacerbate autophagic flux in established malignancies, promoting tumor cell proliferation, migration, metastasis, and resistance to therapeutic interventions. Pro-survival autophagy inhibition may be a promising treatment option for advanced cancer. Furthermore, excessive or persistent autophagy is cytotoxic, resulting in tumor cell death. Targeted autophagy activation has also shown significant promise in the fight against tumor drug resistance. Several research groups have examined the

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Nirosha Yalamandala, Bhanu, Pin-Hua Chen, Thrinayan Moorthy, Thi My Hue Huynh, Wen-Hsuan Chiang, and Shang-Hsiu Hu. "Programmed Catalytic Therapy-Mediated ROS Generation and T-Cell Infiltration in Lung Metastasis by a Dual Metal-Organic Framework (MOF) Nanoagent." Pharmaceutics 14, no. 3 (2022): 527. http://dx.doi.org/10.3390/pharmaceutics14030527.

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Nano-catalytic agents actuating Fenton-like reaction in cancer cells cause intratumoral generation of reactive oxygen species (ROS), allowing the potential for immune therapy of tumor metastasis via the recognition of tumor-associated antigens. However, the self-defense mechanism of cancer cells, known as autophagy, and unsustained ROS generation often restricts efficiency, lowering the immune attack, especially in invading metastatic clusters. Here, a functional core-shell metal-organic framework nanocube (dual MOF) doubling as a catalytic agent and T cell infiltration inducer that programs R

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Ostendorf, Benjamin N., and Sohail F. Tavazoie. "Autophagy Suppresses Breast Cancer Metastasis." Developmental Cell 52, no. 5 (2020): 542–44. http://dx.doi.org/10.1016/j.devcel.2020.02.005.

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Zhang, Jing, Zuozhang Yang, Lin Xie, Lei Xu, Da Xu, and Xuefeng Liu. "Statins, autophagy and cancer metastasis." International Journal of Biochemistry & Cell Biology 45, no. 3 (2013): 745–52. http://dx.doi.org/10.1016/j.biocel.2012.11.001.

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Jalouli, Maroua. "Emerging Role of Hypoxia-Inducible Factors (HIFs) in Modulating Autophagy: Perspectives on Cancer Therapy." International Journal of Molecular Sciences 26, no. 4 (2025): 1752. https://doi.org/10.3390/ijms26041752.

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Hypoxia-inducible factors (HIFs) are master regulators of cellular responses to low oxygen levels and modulate autophagy, a conserved process essential for maintaining homeostasis. Under hypoxic conditions, HIFs regulate the expression of autophagy-related genes and influence autophagic flux and cellular stress responses. Dysregulated hypoxia-induced autophagy promotes cancer cell survival, metabolism, and metastasis, thereby contributing to treatment resistance. Targeting HIF-mediated pathways or modulating autophagic processes offers the potential to improve traditional cancer therapies and

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Zhu, Lucía, Natalia Yebra, Diana Retana, et al. "42. IDENTIFICATION OF BRAIN METASTASIS VULNERABILITIES USING METPLATFORM." Neuro-Oncology Advances 2, Supplement_2 (2020): ii8. http://dx.doi.org/10.1093/noajnl/vdaa073.030.

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Abstract The diagnosis of brain metastasis involves high morbidity and mortality and remains an unmet clinical need in spite of being the most common tumor in the brain. Exclusion of these cancer patients from clinical trials is a major cause of their limited therapeutic options. In this study, we report a novel drug-screening platform (METPlatform) based on organotypic cultures which allows identifying effective anti-metastasis agents in the presence of the organ microenvironment. We have applied this approach to clinically relevant stages of brain metastasis using both experimental models an

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Ryabaya, O. O., and A. A. Prokofieva. "The interplay of autophagy and epithelial-to-mesenchymal transition in cancer progression." Advances in Molecular Oncology 7, no. 2 (2020): 8–19. http://dx.doi.org/10.17650/2313-805x-2020-7-2-8-19.

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Autophagy and epithelial-to-mesenchymal transition (EMT) are the main biological processes involved in tumor progression, and are closely linked. On the one hand, activation of autophagy provides energy and essential nutrients for EMT during the metastases spreading, which is required for tumor cells survival in adverse environmental conditions. On the other hand, autophagy, acting as a tumor suppressor, tends to inhibit metastasis by selectively suppressing the transcription factors of EMT in the early stages. Therefore, inhibition of EMT by inhibitors or inducers of autophagy may be a new st

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Sheng, Xia, Pengfei Zhu, Yi Zhao, et al. "Effect of PI3K/AKT/mTOR Signaling Pathway on Regulating and Controlling the Anti-Invasion and Metastasis of Hepatoma Cells by Bufalin." Recent Patents on Anti-Cancer Drug Discovery 16, no. 1 (2021): 54–65. http://dx.doi.org/10.2174/1574892816666210201120324.

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Background: Autophagy plays a “double-edged sword” in the process of tumorigenesis, development and metastasis. Objective: In this study, we explored the effect of PI3K/AKT/mTOR autophagy-related signaling pathway on regulating and controlling the invasion and metastasis of liver cancer cells by Bufalin. Methods: The cell counting, migration, adhesion and invasion assay were used to evaluate the effect of Bufalin on cell proliferation, invasion and metastasis. The protein expression of PI3K/AKT/ mTOR signaling pathway were detected by the Western Blotting technique. Results: After inhibiting a

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Jahangiri, Leila. "Metastasis in Neuroblastoma and Its Link to Autophagy." Life 13, no. 3 (2023): 818. http://dx.doi.org/10.3390/life13030818.

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Neuroblastoma is a paediatric malignancy originating from the neural crest that commonly occurs in the abdomen and adrenal gland, leading to cancer-related deaths in children. Distant metastasis can be encountered at diagnosis in greater than half of these neuroblastoma patients. Autophagy, a self-degradative process, plays a key role in stress-related responses and the survival of cells and has been studied in neuroblastoma. Accordingly, in the early stages of metastasis, autophagy may suppress cancer cell invasion and migration, while its role may be reversed in later stages, and it may faci

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Mengual, Daniela, Luz Elena Medrano, Wendy Villamizar-Villamizar, Estefanie Osorio-Llanes, Evelyn Mendoza-Torres, and Samir Bolívar. "Novel Effects of Statins on Cancer via Autophagy." Pharmaceuticals 15, no. 6 (2022): 648. http://dx.doi.org/10.3390/ph15060648.

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Cancer is one of the main causes of death globally. Most of the molecular mechanisms underlying cancer are marked by complex aberrations that activate the critical cell-signaling pathways that play a pivotal role in cell metabolism, tumor development, cytoskeletal reorganization, and metastasis. The phosphatidylinositol 3-kinase/protein kinase-B/mammalian target of the rapamycin (PI3K/AKT/mTOR) pathway is one of the main signaling pathways involved in carcinogenesis and metastasis. Autophagy, a cellular pathway that delivers cytoplasmic components to lysosomes for degradation, plays a dual rol

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Guo, Ziyuan, Yang Chen, Yaran Wu, and Jiqin Lian. "CircRNA regulates the liquid-liquid phase separation of ATG4B, a novel strategy to inhibit cancer metastasis?" Cell Stress 8 (2024): 56–58. http://dx.doi.org/10.15698/cst2024.05.296.

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Anoikis is a common programmed death for most of detached cells, but cancer cells can obtain anoikis resistance to facilitate their distant metastasis through the circulation system. Researches have indicated that enhanced autophagic flux accounts for the survival of many cancer cells under detached conditions. Targeting ATG4B, the key factor of autophagy progress, can inhibit cancer metastasis in vitro, but ATG4B-deficient mice are susceptible to many serious diseases, which indicates the potential uncontrolled side effects of direct targeting of ATG4B. In our recent research, we confirmed th

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Zhang, Hao, Kun Zhu, Xue-Feng Zhang та ін. "Pachymic acid exerts antitumor activities by modulating the Wnt/β-catenin signaling pathway via targeting PTP1B". Asian Pacific Journal of Tropical Biomedicine 14, № 4 (2024): 170–80. http://dx.doi.org/10.4103/apjtb.apjtb_857_23.

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Objective: To determine the inhibitory effects of pachymic acid on lung adenocarcinoma (LUAD) cells and elucidate its underlying mechanism. Methods: CCK-8, wound healing, Transwell, Western blot, tube formation, and immunofluorescence assays were carried out to measure the effects of various concentrations of pachymic acid on LUAD cell proliferation, metastasis, angiogenesis as well as autophagy. Subsequently, molecular docking technology was used to detect the potential targeted binding association between pachymic acid and protein tyrosine phosphatase 1B (PTP1B). Moreover, PTP1B was overexpr

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Zada, Sahib, Jin Hwang, Mahmoud Ahmed, Trang Lai, Trang Pham, and Deok Kim. "Control of the Epithelial-to-Mesenchymal Transition and Cancer Metastasis by Autophagy-Dependent SNAI1 Degradation." Cells 8, no. 2 (2019): 129. http://dx.doi.org/10.3390/cells8020129.

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Autophagy, an intracellular degradation process, is essential for maintaining cell homeostasis by removing damaged organelles and proteins under various conditions of stress. In cancer, autophagy has conflicting functions. It plays a key role in protecting against cancerous transformation by maintaining genomic stability against genotoxic components, leading to cancerous transformation. It can also promote cancer cell survival by supplying minimal amounts of nutrients during cancer progression. However, the molecular mechanisms underlying how autophagy regulates the epithelial-to-mesenchymal t

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Yun, Chul Won, Juhee Jeon, Gyeongyun Go, Jun Hee Lee, and Sang Hun Lee. "The Dual Role of Autophagy in Cancer Development and a Therapeutic Strategy for Cancer by Targeting Autophagy." International Journal of Molecular Sciences 22, no. 1 (2020): 179. http://dx.doi.org/10.3390/ijms22010179.

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Autophagy is a delicate intracellular degradation process that occurs due to diverse stressful conditions, including the accumulation of damaged proteins and organelles as well as nutrient deprivation. The mechanism of autophagy is initiated by the creation of autophagosomes, which capture and encapsulate abnormal components. Afterward, autophagosomes assemble with lysosomes to recycle or remove degradative cargo. The regulation of autophagy has bipolar roles in cancer suppression and promotion in diverse cancers. Furthermore, autophagy modulates the features of tumorigenesis, cancer metastasi

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Poornimaa, Murali, and Karuppasamy Ramanathan. "The role of autophagy for cancer treatment: A systematic review." Research Journal of Chemistry and Environment 25, no. 8 (2022): 147–67. http://dx.doi.org/10.25303/258rjce147167.

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Autophagy is a highly conserved catabolic process that regulates nutrient deprivation and metabolic stress through lysosomal degradation. In addition, autophagy is also identified to regulate various processes such as maintaining cellular homeostasis, conserving genomic stability, immunity, inflammation and quality control. The dysregulation of autophagy promotes the development of various diseases such as obesity, diabetes, neurodegenerative disease and cancer. However, autophagy expresses a dichotomous role in cancer. During the initial stage of malignancy, autophagy acts as a suppressor. Ne

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Seok, Jin Kyung, Eun-Hee Hong, Gabsik Yang, et al. "Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy." Cells 10, no. 3 (2021): 558. http://dx.doi.org/10.3390/cells10030558.

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Oxidized phospholipids are well known to play physiological and pathological roles in regulating cellular homeostasis and disease progression. However, their role in cancer metastasis has not been entirely understood. In this study, effects of oxidized phosphatidylcholines such as 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) on epithelial-mesenchymal transition (EMT) and autophagy were determined in cancer cells by immunoblotting and confocal analysis. Metastasis was analyzed by a scratch wound assay and a transwell migration/invasion assay. The concentrations of POVPC and

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Zhu, Lucía, Carmen Blanco-Aparicio, Luca Bertero, et al. "BSCI-02. METPlatform identifies brain metastasis vulnerabilities and predicts patient response to therapy." Neuro-Oncology Advances 3, Supplement_3 (2021): iii1. http://dx.doi.org/10.1093/noajnl/vdab071.001.

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Abstract The diagnosis of brain metastasis involves high morbidity and mortality and remains an unmet clinical need in spite of being the most common tumor in the brain. Exclusion of these cancer patients from clinical trials is a major cause of their limited therapeutic options. We report a novel drug-screening platform (METPlatform) based on organotypic cultures which allows identifying effective anti-metastasis agents in the presence of the organ microenvironment. By applying this approach to brain metastasis, we identified heat shock protein 90 (HSP90) as a promising therapeutic target for

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Su, Zhenyi, Zuozhang Yang, Yongqing Xu, Yongbin Chen, and Qiang Yu. "Apoptosis, autophagy, necroptosis, and cancer metastasis." Molecular Cancer 14, no. 1 (2015): 48. http://dx.doi.org/10.1186/s12943-015-0321-5.

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Cabrera-Serrano, Antonio José, José Manuel Sánchez-Maldonado, Carmen González-Olmedo, et al. "Crosstalk Between Autophagy and Oxidative Stress in Hematological Malignancies: Mechanisms, Implications, and Therapeutic Potential." Antioxidants 14, no. 3 (2025): 264. https://doi.org/10.3390/antiox14030264.

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Autophagy is a fundamental cellular process that maintains homeostasis by degrading damaged components and regulating stress responses. It plays a crucial role in cancer biology, including tumor progression, metastasis, and therapeutic resistance. Oxidative stress, similarly, is key to maintaining cellular balance by regulating oxidants and antioxidants, with its disruption leading to molecular damage. The interplay between autophagy and oxidative stress is particularly significant, as reactive oxygen species (ROS) act as both inducers and by-products of autophagy. While autophagy can function

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Eng, Gracie Wee Ling, Yilong Zheng, Dominic Wei Ting Yap, Andrea York Tiang Teo, and Jit Kong Cheong. "Autophagy and ncRNAs: Dangerous Liaisons in the Crosstalk between the Tumor and Its Microenvironment." Cancers 14, no. 1 (2021): 20. http://dx.doi.org/10.3390/cancers14010020.

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Autophagy is a fundamental cellular homeostasis mechanism known to play multifaceted roles in the natural history of cancers over time. It has recently been shown that autophagy also mediates the crosstalk between the tumor and its microenvironment by promoting the export of molecular payloads such as non-coding RNA (ncRNAs) via LC3-dependent Extracellular Vesicle loading and secretion (LDELS). In turn, the dynamic exchange of exosomal ncRNAs regulate autophagic responses in the recipient cells within the tumor microenvironment (TME), for both tumor and stromal cells. Autophagy-dependent pheno

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Manganelli, Valeria, Roberta Misasi, Gloria Riitano, et al. "Role of a Novel Heparanase Inhibitor on the Balance between Apoptosis and Autophagy in U87 Human Glioblastoma Cells." Cells 12, no. 14 (2023): 1891. http://dx.doi.org/10.3390/cells12141891.

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Background: Heparanase (HPSE) is an endo-β-glucuronidase that cleaves heparan sulfate side chains, leading to the disassembly of the extracellular matrix, facilitating cell invasion and metastasis dissemination. In this research, we investigated the role of a new HPSE inhibitor, RDS 3337, in the regulation of the autophagic process and the balance between apoptosis and autophagy in U87 glioblastoma cells. Methods: After treatment with RDS 3337, cell lysates were analyzed for autophagy and apoptosis-related proteins by Western blot. Results: We observed, firstly, that LC3II expression increased

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Santana-Codina, Naiara, Laia Muixí, Ruben Foj, et al. "GRP94 promotes brain metastasis by engaging pro-survival autophagy." Neuro-Oncology 22, no. 5 (2019): 652–64. http://dx.doi.org/10.1093/neuonc/noz198.

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Abstract Background GRP94 is a glucose-regulated protein critical for survival in endoplasmic reticulum stress. Expression of GRP94 is associated with cellular transformation and increased tumorigenicity in breast cancer. Specifically, overexpression of GRP94 predicts brain metastasis (BM) in breast carcinoma patients with either triple negative or ErbB2 positive tumors. The aim of this study was to understand if microenvironmental regulation of GRP94 expression might be a hinge orchestrating BM progression. Methods GRP94 ablation was performed in a BM model BR-eGFP-CMV/Luc-V5CA1 (BRV5CA1) of

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Vtorushin, S. V., K. V. Rachkovsky, N. V. Krakhmal, I. V. Stepanov, and M. V. Zavyalova. "A LINK BETWEEN AUTOPHAGY REGULATORY PROTEINS M-TOR AND BECLIN-1 AND PARAMETERS OF LYMPHOGENIC METASTASIS IN COLORECTAL CANCER." Siberian journal of oncology 17, no. 4 (2018): 41–47. http://dx.doi.org/10.21294/1814-4861-2018-17-4-41-47.

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Currently the impact of autophagy on carcinogenesis remains understudied. On the one hand, autophagy acts as a tumor suppressor, as it activates degradation of oncoproteins, toxic proteins, and damaged cell organelles, that may be aggressive and lead to DNA damage. On the other hand, autophagy may promote tumor cell survival under hypoxia and in the presence of reactive oxygen species, which occurs primarily due to blocking of apoptosis mechanisms, raising the chances for maintaining tumor clone dynamics. Autophagy regulation is a complicated and multi-stage process. The main regulator here is

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Zhu, L., C. Blanco-Aparicio, L. Bertero, et al. "OS06.7A METPlatform identifies brain metastasis vulnerabilities and predicts patient response to therapy." Neuro-Oncology 23, Supplement_2 (2021): ii10. http://dx.doi.org/10.1093/neuonc/noab180.031.

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Abstract BACKGROUND The diagnosis of brain metastasis involves high morbidity and mortality and remains an unmet clinical need in spite of being the most common tumor in the brain. Exclusion of these cancer patients from clinical trials is a major cause of their limited therapeutic options. MATERIAL AND METHODS We report a novel drug-screening platform (METPlatform) based on organotypic cultures which allows identifying effective anti-metastasis agents in the presence of the organ microenvironment. We have applied this approach to clinically relevant stages of brain metastasis using both exper

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Lee, Yoon-Seung, Jeong-Geon Mun, Shin-Young Park, et al. "Saikosaponin D Inhibits Lung Metastasis of Colorectal Cancer Cells by Inducing Autophagy and Apoptosis." Nutrients 16, no. 12 (2024): 1844. http://dx.doi.org/10.3390/nu16121844.

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Saikosaponin D (SSD), derived from Bupleurum falcatum L., has various pharmacological properties, including immunoregulatory, anti-inflammatory, and anti-allergic effects. Several studies have investigated the anti-tumor effects of SSD on cancer in multiple organs. However, its role in colorectal cancer (CRC) remains unclear. Therefore, this study aimed to elucidate the suppressive effects of SSD on CRC cell survival and metastasis. SSD reduced the survival and colony formation ability of CRC cells. SSD-induced autophagy and apoptosis in CRC cells were measured using flow cytometry. SSD treatm

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Kawakita, Emi, Fan Yang, Sen Shi, Yuta Takagaki, Daisuke Koya та Keizo Kanasaki. "Inhibition of Dipeptidyl Peptidase-4 Activates Autophagy to Promote Survival of Breast Cancer Cells via the mTOR/HIF-1α Pathway". Cancers 15, № 18 (2023): 4529. http://dx.doi.org/10.3390/cancers15184529.

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Autophagy plays a complex role in breast cancer cell survival, metastasis, and chemotherapeutic resistance. Dipeptidyl peptidase (DPP)-4, a therapeutic target for type 2 diabetes mellitus, is also involved in autophagic flux. The potential influence of DPP-4 suppression on cancer biology remains unknown. Here, we report that DPP-4 deficiency promotes breast cancer cell survival via the induction of autophagy by the C-X-C motif chemokine 12 (CXCL12)/C-X-C receptor 4 (CXCR4)/mammalian target of rapamycin (mTOR)/hypoxia inducible factor (HIF)-1α axis. DPP-4 knockdown and DPP-4 inhibitor KR62436 (

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Matrood, Sami, Leander Edwin Melms, Detlef Klaus Bartsch, and Pietro Di Fazio. "The Expression of Autophagy-Associated Genes Represents a Valid Footprint for Aggressive Pancreatic Neuroendocrine Neoplasms." International Journal of Molecular Sciences 24, no. 4 (2023): 3636. http://dx.doi.org/10.3390/ijms24043636.

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Pancreatic neuroendocrine neoplasms (pNEN) are rare and heterogeneous tumors. Previous investigations have shown that autophagy can be a target for cancer therapy. This study aimed to determine the association between the expression of autophagy-associated gene transcripts and clinical parameters in pNEN. In total, 54 pNEN specimens were obtained from our human biobank. The patient characteristics were retrieved from the medical record. RT-qPCR was performed to assess the expression of the autophagic transcripts BECN1, MAP1LC3B, SQSTM1, UVRAG, TFEB, PRKAA1, and PRKAA2 in the pNEN specimens. A

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Kim, Jin-Wook, Feriel Mahiddine, and Geon Kim. "Leptin Modulates the Metastasis of Canine Inflammatory Mammary Adenocarcinoma Cells through Downregulation of Lysosomal Protective Protein Cathepsin A (CTSA)." International Journal of Molecular Sciences 21, no. 23 (2020): 8963. http://dx.doi.org/10.3390/ijms21238963.

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Canine malignant mammary gland tumors present with a poor prognosis due to metastasis to other organs, such as lung and lymph node metastases. Unlike in human studies where obesity has been shown to increase the risk of breast cancer, this has not been well studied in veterinary science. In our preliminary study, we discovered that leptin downregulated cathepsin A, which is responsible for lysosomal-associated membrane protein 2a (LAMP2a) degradation. LAMP2a is a rate-limiting factor in chaperone-mediated autophagy and is highly active in malignant cancers. Therefore, in this study, alteration

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Rahman, Md Ataur, Abu Saim Mohammad Saikat, Md Saidur Rahman, Mobinul Islam, Md Anowar Khasru Parvez, and Bonglee Kim. "Recent Update and Drug Target in Molecular and Pharmacological Insights into Autophagy Modulation in Cancer Treatment and Future Progress." Cells 12, no. 3 (2023): 458. http://dx.doi.org/10.3390/cells12030458.

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Recent evidence suggests that autophagy is a governed catabolic framework enabling the recycling of nutrients from injured organelles and other cellular constituents via a lysosomal breakdown. This mechanism has been associated with the development of various pathologic conditions, including cancer and neurological disorders; however, recently updated studies have indicated that autophagy plays a dual role in cancer, acting as a cytoprotective or cytotoxic mechanism. Numerous preclinical and clinical investigations have shown that inhibiting autophagy enhances an anticancer medicine’s effectiv

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Hait, Nitai, APARNA MAITI, Rongrong Wu, Kazuaki Takabe, and Masanori Oshi. "Abstract 5653: Increased expression of brain-specific serine/threonine-protein kinase BRSK2 contributes to breast cancer survival by enhancing autophagy under nutrient stress." Cancer Research 82, no. 12_Supplement (2022): 5653. http://dx.doi.org/10.1158/1538-7445.am2022-5653.

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Abstract Aberrant expression of certain cancer-promoting genes is the associative factor of metastasis and cancer-related death. Autophagy is a highly conserved catabolic process that can be regulated by starvation or stress. Among several cellular stresses, hypoxia and nutrient stress can strongly activate autophagy-related genes. Autophagy plays dual roles in cancer; it can be pro-death or pro-survival. The ability of the cancer cells to survive long-term under stress is still a vast question to cancer researchers. The nutrient status of is sensed by LKB1 downstream kinases AMP-activated pro

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Kumar, Aviral, Sosmitha Girisa, Mohammed S. Alqahtani, et al. "Targeting Autophagy Using Long Non-Coding RNAs (LncRNAs): New Landscapes in the Arena of Cancer Therapeutics." Cells 12, no. 5 (2023): 810. http://dx.doi.org/10.3390/cells12050810.

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Cancer has become a global health hazard accounting for 10 million deaths in the year 2020. Although different treatment approaches have increased patient overall survival, treatment for advanced stages still suffers from poor clinical outcomes. The ever-increasing prevalence of cancer has led to a reanalysis of cellular and molecular events in the hope to identify and develop a cure for this multigenic disease. Autophagy, an evolutionary conserved catabolic process, eliminates protein aggregates and damaged organelles to maintain cellular homeostasis. Accumulating evidence has implicated the

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Chen, Yan, Chengxing Xia, Chunwei Ye, et al. "MT-12 inhibits the proliferation of bladder cells in vitro and in vivo by enhancing autophagy through mitochondrial dysfunction." Open Life Sciences 17, no. 1 (2022): 710–25. http://dx.doi.org/10.1515/biol-2022-0082.

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Abstract Bladder cancer (BC) is one of the most common malignancies involving the urinary system. Our previous study demonstrated that cobra venom membrane toxin 12 (MT-12) could effectively inhibit BC cell growth and metastasis and induce apoptosis. However, the specific molecular mechanism remains unknown. In this study, we explored whether MT-12 inhibits BC cell proliferation by inducing autophagy cell death through mitochondrial dysfunction. As a result, MT-12 inhibited proliferation and colony formation in RT4 and T24 cells. In the BC xenograft mouse model, autophagy inhibitor 3-MA allevi

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Gorabi, Armita Mahdavi, Nasim Kiaie, Saeed Aslani, Thozhukat Sathyapalan, Tannaz Jamialahmadi, and Amirhossein Sahebkar. "Implications on the Therapeutic Potential of Statins via Modulation of Autophagy." Oxidative Medicine and Cellular Longevity 2021 (July 30, 2021): 1–10. http://dx.doi.org/10.1155/2021/9599608.

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Statins, which are functionally known as 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) inhibitors, are lipid-lowering compounds widely prescribed in patients with cardiovascular diseases (CVD). Several biological and therapeutic functions have been attributed to statins, including neuroprotection, antioxidation, anti-inflammation, and anticancer effects. Pharmacological characteristics of statins have been attributed to their involvement in the modulation of several cellular signaling pathways. Over the past few years, the therapeutic role of statins has partially been attributed to the induction

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Mazitova, A. M., Iu A. Topchu, L. A. Mingazova, E. M. Biktagirova, Z. I. Abramova, and R. T. Gabbasov. "Role of autophagy in response of epithelial ovarian cancer cells to cisplatin treatment and cisplatin resistance." Genes & Cells 15, no. 3 (2020): 44–47. http://dx.doi.org/10.23868/202011006.

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Ovarian cancer survival rate is inversely associated with the extent of tumor metastasis. One of the main treatment approaches against ovarian cancer is employment of platinum based therapies, including cisplatin. Majority of ovarian cancer patients develop cisplatin resistance. We aimed to investigate roles for macroautophagy in response of epithelial ovarian cancer cells to cisplatin, including changes in cell motility, as well as in development of cisplatin resistance. Cisplatin treatment induced autophagy in Caov-3 cells in vitro, as well as resulted in increased cell motility. Pharmacolog

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Wang, Xin, Jihye Lee, and Changqing Xie. "Autophagy Regulation on Cancer Stem Cell Maintenance, Metastasis, and Therapy Resistance." Cancers 14, no. 2 (2022): 381. http://dx.doi.org/10.3390/cancers14020381.

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Cancer stem cells (CSCs) are a subset of the tumor population that play critical roles in tumorigenicity, metastasis, and relapse. A key feature of CSCs is their resistance to numerous therapeutic strategies which include chemotherapy, radiation, and immune checkpoint inhibitors. In recent years, there is a growing body of literature that suggests a link between CSC maintenance and autophagy, a mechanism to recycle intracellular components during moments of environmental stress, especially since CSCs thrive in a tumor microenvironment that is plagued with hypoxia, acidosis, and lack of nutrien

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Begum, Rizwana, Shilpa Thota, Dhirendra Pratap Singh, et al. "Abstract 4775: Unveiling caveolin-1's crucial role in breast cancer progression and metastasis: A molecular perspective." Cancer Research 84, no. 6_Supplement (2024): 4775. http://dx.doi.org/10.1158/1538-7445.am2024-4775.

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Abstract Background: Breast cancer, particularly its metastatic form, constitutes a significant portion of oncological mortality. Caveolin-1 (Cav-1), a caveolae structural protein, has been implicated in cellular processes such as proliferation, apoptosis, autophagy, and cellular motility (aberrant in breast cancer). With its dual role as a tumor suppressor and promoter, Cav-1's function in breast cancer pathophysiology requires elucidation for potential therapeutic targeting. Methods: We utilized a syngeneic mouse model to engineer Cav-1 deficient 4T1 murine mammary carcinoma cells which mirr

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Alizadeh, Javad, Shahrokh Lorzadeh, and Saeid Ghavami. "Autophagy and cancer metastasis: a Trojan horse." Journal of Investigative Medicine 69, no. 6 (2021): 1145–47. http://dx.doi.org/10.1136/jim-2021-002016.

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Kenific, Candia M., Andrew Thorburn, and Jayanta Debnath. "Autophagy and metastasis: another double-edged sword." Current Opinion in Cell Biology 22, no. 2 (2010): 241–45. http://dx.doi.org/10.1016/j.ceb.2009.10.008.

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Tang, Hao, Shida Zhu, Kai Chen, Shujie Yuan, Junzu Hu, and Hongkai Wang. "IL-17A regulates autophagy and promotes osteoclast differentiation through the ERK/mTOR/Beclin1 pathway." PLOS ONE 18, no. 2 (2023): e0281845. http://dx.doi.org/10.1371/journal.pone.0281845.

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Bone is a frequent target of tumor metastasis, with high incidence rate and poor prognosis. Osteoclasts play a key role in the process of tumor bone metastasis. Interleukin-17A (IL-17A) is an inflammatory cytokine, highly expressed in a variety of tumor cells, that can alter the autophagic activity of other cells, thereby causing corresponding lesions. Previous studies have shown that low concentration IL-17A can promote osteoclastogenesis. The aim of this study was to clarify the mechanism of low concentration IL-17A promoting osteoclastogenesis by regulating autophagic activity. The results

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Arif, Amin, Muhammad Babar Khawar, Rabia Mehmood, Muddasir Hassan Abbasi, and Nadeem Sheikh. "Dichotomous role of autophagy in cancer." Asian Biomedicine 16, no. 3 (2022): 111–20. http://dx.doi.org/10.2478/abm-2022-0014.

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Abstract Autophagy is an evolutionary conserved catabolic process that plays physiological and pathological roles in a cell. Its effect on cellular metabolism, the proteome, and the number and quality of organelles, diversely holds the potential to alter cellular functions. It acts paradoxically in cancer as a tumor inhibitor as well as a tumor promoter. In the early stage of tumorigenesis, it prevents tumor initiation by the so-called “quality control mechanism” and suppresses cancer progression. For late-staged tumors that are exposed to stress, it acts as a vibrant process of degradation an

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Chen, Yu-Ying, Chun-Hsien Chen, Wei-Chen Lin, et al. "The Role of Autophagy in Anti-Cancer and Health Promoting Effects of Cordycepin." Molecules 26, no. 16 (2021): 4954. http://dx.doi.org/10.3390/molecules26164954.

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Cordycepin is an adenosine derivative isolated from Cordyceps sinensis, which has been used as an herbal complementary and alternative medicine with various biological activities. The general anti-cancer mechanisms of cordycepin are regulated by the adenosine A3 receptor, epidermal growth factor receptor (EGFR), mitogen-activated protein kinases (MAPKs), and glycogen synthase kinase (GSK)-3β, leading to cell cycle arrest or apoptosis. Notably, cordycepin also induces autophagy to trigger cell death, inhibits tumor metastasis, and modulates the immune system. Since the dysregulation of autophag

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