Journal articles: 'Forkhead Box Protein O1'

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Zhu, Wan Long, Honglian Tong, Jing Tsong Teh, and Mei Wang. "Forkhead Box Protein O3 Transcription Factor Negatively Regulates Autophagy in Human Cancer Cells by Inhibiting Forkhead Box Protein O1 Expression and Cytosolic Accumulation." PLoS ONE 9, no. 12 (December 29, 2014): e115087. http://dx.doi.org/10.1371/journal.pone.0115087.

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Stenman, Adam, Timothy Murtha, Reju Korah, and Tobias Carling. "Suppression of Forkhead Box Protein O1 (FOXO1) Transcription Factor May Promote Adrenocortical Tumorigenesis." Hormone and Metabolic Research 49, no. 08 (June 22, 2017): 631–37. http://dx.doi.org/10.1055/s-0043-110143.

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AbstractDespite recent comprehensive genetic analyses, molecular evidence for a pathophysiological continuum linking benign adrenocortical adenoma (ACA) and highly aggressive adrenocortical carcinoma (ACC) is still elusive. Using human tumor samples and the established ACC cell line SW-13, this study investigated potential regulatory roles for FOXO transcription factors, in modulating adrenocortical tumorigenesis. Adrenocortical tumor specimens (20 ACAs, 10 ACCs, and 9 normal adrenal tissue samples) obtained from 30 patients were analyzed for ubiquitously expressed FOXO transcription factors, FOXO1 and FOXO3 using qRT-PCR and immunohistochemistry. The SW-13 ACC cells were used to study the phenotypic effects of FOXO regulation in vitro. While FOXO3 expression remained unchanged in ACCs, FOXO1 expression was found to be significantly downregulated in 19/20 ACAs and 9/10 ACCs (p<0.0001 and p<0.05, respectively), suggesting a global role for FOXO1 suppression in promoting and maintaining adrenocortical dedifferentiation. Silencing of FOXO1 in SW-13 cells resulted in significant loss of viability (p<0.001) mediated by apoptosis as determined by quantitative Annexin V immunofluorescence analysis (p<0.01). FOXO1 silencing also augmented the migratory behavior of SW-13 cells (p<0.0001), suggesting distinct roles for FOXO1 in promoting viability and controlled motility of adrenocortical cells.

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Chen, Qing, Mingjian Lu, Bobby R. Monks, and Morris J. Birnbaum. "Insulin Is Required to Maintain Albumin Expression by Inhibiting Forkhead Box O1 Protein." Journal of Biological Chemistry 291, no. 5 (December 14, 2015): 2371–78. http://dx.doi.org/10.1074/jbc.m115.677351.

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Han, G. H., D. Chung, D. B. Chay, H. Cho, S. Kim, and J. H. Kim. "Prognostic assessment of forkhead box protein O1 (FOXO1) and paired box 3 (PAX3) in epithelial ovarian cancer." Gynecologic Oncology 159 (October 2020): 113. http://dx.doi.org/10.1016/j.ygyno.2020.05.123.

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Wang, Ying, Jing Tong, Dawei Zou, Bing Chang, Baifang Wang, and Bingyuan Wang. "Elevated expression of forkhead box protein O1 (FoxO1) in alcohol-induced intestinal barrier dysfunction." Acta Histochemica 115, no. 6 (July 2013): 557–63. http://dx.doi.org/10.1016/j.acthis.2012.12.005.

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Zhang, Xiaojun, Lusheng Jiang, and Huimin Liu. "Forkhead Box Protein O1: Functional Diversity and Post-Translational Modification, a New Therapeutic Target?" Drug Design, Development and Therapy Volume 15 (May 2021): 1851–60. http://dx.doi.org/10.2147/dddt.s305016.

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Ward, Erin C., Anna V. Hoekstra, Leen J. Blok, P. Hanifi-Moghaddam, John R. Lurain, Diljeet K. Singh, Barbara M. Buttin, Julian C. Schink, and J. Julie Kim. "The Regulation and Function of the Forkhead Transcription Factor, Forkhead Box O1, Is Dependent on the Progesterone Receptor in Endometrial Carcinoma." Endocrinology 149, no. 4 (December 20, 2007): 1942–50. http://dx.doi.org/10.1210/en.2007-0756.

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In many type I endometrial cancers, the PTEN gene is inactivated, which ultimately leads to constitutively active Akt and the inhibition of Forkhead box O1 (FOXO1), a member of the FOXO subfamily of Forkhead/winged helix family of transcription factors. The expression, regulation, and function of FOXO1 in endometrial cancer were investigated in this study. Immunohistochemical analysis of 49 endometrial tumor tissues revealed a decrease of FOXO1 expression in 95.9% of the cases compared with the expression in normal endometrium. In four different endometrial cancer cell lines (ECC1, Hec1B, Ishikawa, and RL95), FOXO1 mRNA was expressed at similar levels; however, protein levels were low or undetectable in Ecc1, Ishikawa, and RL95 cells. Using small interfering RNA technology, we demonstrated that the low levels of FOXO1 protein were due to the involvement of Skp2, an oncogenic subunit of the Skp1/Cul1/F-box protein ubiquitin complex, given that silencing Skp2 increased FOXO1 protein expression in Ishikawa cells. Inhibition of Akt in Ishikawa cells also increased nuclear FOXO1 protein levels. Additionally, progestins increased FOXO1 protein levels, specifically through progesterone receptor B (PRB) as determined by using stably transfected PRA-specific and PRB-specific Ishikawa cell lines. Finally, overexpression of triple mutant (Tm) FOXO1 in the PR-specific Ishikawa cell lines caused cell cycle arrest and significantly decreased proliferation in the presence and absence of the progestin, R5020. Furthermore, TmFOXO1 overexpression induced apoptosis in PRB-specific cells in the presence and absence of ligand. Taken together, these data provide insight into the phosphoinositide-3-kinase/Akt/FOXO pathway for the determination of progestin responsiveness and the development of alternate therapies for endometrial cancer.

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Cho, Hanbyoul, Gwan Hee Han, and Jae-Hoon Kim. "Prognostic implication of forkhead box protein O1 (FOXO1) and paired box gene 3 (PAX3) in epithelial ovarian cancer." Journal of Global Oncology 5, suppl (October 7, 2019): 61. http://dx.doi.org/10.1200/jgo.2019.5.suppl.61.

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61 Background: Transcriptional factor, Forkhead box protein O1 (FOXO1) has been reported to play an imported role in human cancer, but the role in epithelial ovarian cancer (EOC) has not yet been clarified. Here, we evaluatedthe expression and clinical significance of FOXO1 in EOC. Methods: Immunohistochemical analyses of FOXO1 and PAX3 in 212 in EOCs, 57 borderline ovarian tumors and 153 benign epithelial ovarian tumors and 79 nonadjacent normal epithelial tissues were performed using tissue microarray analysis. The data were compared with clinicopathological variables including the survival of EOC patients. Also, the effect of FOXO1 on cell growth were assessed in EOC cell lines. Results: The expressions of FOXO1 and PAX3 protein were significantly higher in EOC tissues than in nonadjacent normal epithelial tissues, benign tissues and borderline tumors respectively (all p< 0.001). Overexpression of FOXO1 was significantly associated with poor grade ( p = 0.004). FOXO1 expression showed trend of positive correlation with that of PAX3 in EOC tissues ( Spearman’s rho0.118, p= 0.149). Multivariate survival analysis revealed that the high expression of FOXO1 (hazard ratio = 2.74 [95% CI, 1.22–13.10], p = 0.001) could be an independent prognostic factor for overall survival. Most importantly, high expression of both FOXO1 and PAX3 showed high hazard ratio (hazard ratio = 5.53 [95% CI, 2.47–12.40], p< 0.001) for overall survival. In vitro result revealed that knockdown of FOXO1 was associated decreased cell viability and migration. Conclusions: This study reveals that high expression of FOXO1/PAX3 is an indicator of poor prognosis in EOC. Our results not only suggest the promising potential of FOXO1 and PAX3 as a prognostic and survival marker, but also warrant further studies on a possible link between the biological function of FOXO1 and PAX3 of EOC.

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Di Pietro, Natalia, Valentine Panel, Schantel Hayes, Alessia Bagattin, Sunitha Meruvu, Assunta Pandolfi, Lynne Hugendubler, Geza Fejes-Tóth, Aniko Naray-Fejes-Tóth, and Elisabetta Mueller. "Serum- and Glucocorticoid-Inducible Kinase 1 (SGK1) Regulates Adipocyte Differentiation via Forkhead Box O1." Molecular Endocrinology 24, no. 2 (February 1, 2010): 370–80. http://dx.doi.org/10.1210/me.2009-0265.

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Abstract The serum and glucocorticoid-inducible kinase 1 (SGK1) is an inducible kinase the physiological function of which has been characterized primarily in the kidney. Here we show that SGK1 is expressed in white adipose tissue and that its levels are induced in the conversion of preadipocytes into fat cells. Adipocyte differentiation is significantly diminished via small interfering RNA inhibition of endogenous SGK1 expression, whereas ectopic expression of SGK1 in mesenchymal precursor cells promotes adipogenesis. The SGK1-mediated phenotypic effects on differentiation parallel changes in the mRNA levels for critical regulators and markers of adipogenesis, such as peroxisome proliferator-activated receptor γ, CCAAT enhancer binding protein α, and fatty acid binding protein aP2. We demonstrate that SGK1 affects differentiation by direct phosphorylation of Foxo1, thereby changing its cellular localization from the nucleus to the cytosol. In addition we show that SGK1−/− cells are unable to relocalize Foxo1 to the cytosol in response to dexamethasone. Together these results show that SGK1 influences adipocyte differentiation by regulating Foxo1 phosphorylation and reveal a potentially important function for this kinase in the control of fat mass and function.

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Pfleger, Jessica, Ryan C. Coleman, Jessica Ibetti, Rajika Roy, Ioannis D. Kyriazis, Erhe Gao, Konstantinos Drosatos, and Walter J. Koch. "Genomic Binding Patterns of Forkhead Box Protein O1 Reveal Its Unique Role in Cardiac Hypertrophy." Circulation 142, no. 9 (September 2020): 882–98. http://dx.doi.org/10.1161/circulationaha.120.046356.

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Background: Cardiac hypertrophic growth is mediated by robust changes in gene expression and changes that underlie the increase in cardiomyocyte size. The former is regulated by RNA polymerase II (pol II) de novo recruitment or loss; the latter involves incremental increases in the transcriptional elongation activity of pol II that is preassembled at the transcription start site. The differential regulation of these distinct processes by transcription factors remains unknown. Forkhead box protein O1 (FoxO1) is an insulin-sensitive transcription factor that is also regulated by hypertrophic stimuli in the heart. However, the scope of its gene regulation remains unexplored. Methods: To address this, we performed FoxO1 chromatin immunoprecipitation–deep sequencing in mouse hearts after 7 days of isoproterenol injections (3 mg·kg −1 ·mg −1 ), transverse aortic constriction, or vehicle injection/sham surgery. Results: Our data demonstrate increases in FoxO1 chromatin binding during cardiac hypertrophic growth, which positively correlate with extent of hypertrophy. To assess the role of FoxO1 on pol II dynamics and gene expression, the FoxO1 chromatin immunoprecipitation–deep sequencing results were aligned with those of pol II chromatin immunoprecipitation–deep sequencing across the chromosomal coordinates of sham- or transverse aortic constriction–operated mouse hearts. This uncovered that FoxO1 binds to the promoters of 60% of cardiac-expressed genes at baseline and 91% after transverse aortic constriction. FoxO1 binding is increased in genes regulated by pol II de novo recruitment, loss, or pause-release. In vitro, endothelin-1– and, in vivo, pressure overload–induced cardiomyocyte hypertrophic growth is prevented with FoxO1 knockdown or deletion, which was accompanied by reductions in inducible genes, including Comtd1 in vitro and Fstl1 and Uck2 in vivo. Conclusions: Together, our data suggest that FoxO1 may mediate cardiac hypertrophic growth via regulation of pol II de novo recruitment and pause-release; the latter represents the majority (59%) of FoxO1-bound, pol II–regulated genes after pressure overload. These findings demonstrate the breadth of transcriptional regulation by FoxO1 during cardiac hypertrophy, information that is essential for its therapeutic targeting.

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Zhang, Xiongfei, Wei Yong, Jinghuan Lv, Yunxia Zhu, Jingjing Zhang, Fang Chen, Rihua Zhang, Tao Yang, Yujie Sun, and Xiao Han. "Inhibition of Forkhead Box O1 Protects Pancreatic β-Cells against Dexamethasone-Induced Dysfunction." Endocrinology 150, no. 9 (May 14, 2009): 4065–73. http://dx.doi.org/10.1210/en.2009-0343.

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Abstract Forkhead Box O1 (FoxO1) is a key transcription regulator of insulin/IGF-I signaling pathway, and its activity can be increased by dexamethasone (DEX) in several cell types. However, the role of FoxO1 in DEX-induced pancreatic β-cell dysfunction has not been fully understood. Therefore, in this study, we investigated whether FoxO1 could mediate DEX-induced β-cell dysfunction and the possible underlying mechanisms in pancreatic β-cell line RINm5F cells and primary rat islet. We found that DEX markedly increased FoxO1 mRNA and protein expression and decreased FoxO1 phosphorylation through the Akt pathway, which resulted in an increase in active FoxO1 in RINm5F cells and isolated rat islets. Activated FoxO1 subsequently inhibited pancreatic duodenal homeobox-1 expression and induced nuclear exclusion of pancreatic duodenal homeobox-1. Knockdown of FoxO1 by RNA interference restored the expression of pancreatic duodenal homeobox-1 and prevented DEX-induced dysfunction of glucose-stimulated insulin secretion in rat islets. Together, the results of present study demonstrate that FoxO1 is integrally involved in DEX-induced inhibition of pancreatic duodenal homeobox-1 and glucose-stimulated insulin secretion dysfunction in pancreatic islet β-cells. Inhibition of FoxO1 can effectively protect β-cells against DEX-induced dysfunction.

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Cho, Hanbyoul, Gwan Hee Han, Doo Byung Chay, and Jaehoon Kim. "Association of forkhead box protein O1 and paired box gene 3 overexpression with prognosis in patients with cervical cancer." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e14519-e14519. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14519.

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e14519 Background: Transcriptional factor FOXO1and PAX3 has been reported to play an imported role in human cancer, but the role in cervical cancer has not yet been clarified. Here, we evaluated the functional role of FOXO1 with cervical cancer cells and the expression together with clinical significance of FOXO1 and PAX3 among cervical lesions was investigated. Methods: In vitro assessment of cell functions by cell viably assay, cell migration and invasion assay was evaluated using FOXO1 knockdown cervical cancer cell lines. Immuno-histochemical (IHC) staining analyses of FOXO1 and PAX3 were performed with tissue microarray (TMA) consisting of 209 cervical cancers, 366 high grade cervical intraepithelial neoplasias (CIN), 130 low grade CIN and 328 matched nonadjacent normal cervical epithelial tissues. The clinical significance was investigated by comparing the data with various clinicopathologic characteristics, including survival in cervical cancer. Results: In vitro result revealed that knockdown of FOXO1 was associated decreased cell viability ( p< 0.001), migration ( p< 0.001) and invasion ( p< 0.05) supporting the oncogenic role of FOXO1 in cervical cancer. FOXO1 and PAX3 expression was significantly higher in CIN (both p< 0.001) and cancer tissue (both p< 0.001) than in normal tissue. FOXO1 expression showed significant correlation with PAX3 (Spearman’s rho = 0.377, p< 0.001) in a cervical cancer. Multivariate analysis indicates that FOXO1 expression (hazard ratio = 4.01 [95% CI, 1.22–13.10], p= 0.021) and advanced FIGO stage (hazard ratio = 3.89 [95% CI, 1.35–11.19], p= 0.012) were independent prognostic factor on overall survival. Conclusions: This study reveals the association between FOXO1 and PAX3 expression with clinicopathologic variables, including survival of cervical cancer patients. Our results not only suggest the promising potential of FOXO1 as a prognostic and survival marker, but also warrant further studies on a possible link between the biological function of FOXO1 and the pathogenesis of cervical cancer.

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Fu, Jun-Bao, Zhi-Hua Wang, and Yong-Ying Ren. "Forkhead Box O1-p21 Mediates Macrophage Polarization in Postoperative Cognitive Dysfunction Induced by Sevoflurane." Current Neurovascular Research 17, no. 1 (May 5, 2020): 79–85. http://dx.doi.org/10.2174/1567202617666200128142728.

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Purpose: The current study was conducted in order to investigate the role of Forkhead box O1 and p21-mediated macrophage polarization in postoperative cognitive dysfunction induced by sevoflurane. Methods: There involved a total of 30 healthy mice that were randomly divided into two groups: control group (without any treatment) and anaesthesia group (treated with sevoflurane inhalation). The effects of sevoflurane on cognitive function (memory) in mice were studied by trace fear conditioned reflex, and the effects of systemic inflammation and behavior after operation were measured by enzyme-linked immunosorbent assay (ELISA), the concentrations of CD163 and tumor necrosis factor-α (TNF-α) were measured. The expression of macrophage phenotype was observed by immunofluorescence staining, the expression levels of M1 and M2 markers mRNA were detected by real-time fluorescence quantitative PCR (RT-PCR), and the expression levels of FoxO1 and p21 were analyzed by immunoblotting (Western blot). Results: Compared with the control group, the freezing time in the anesthesia group was lower than that in the control group (P<0.01), indicating that sevoflurane anesthesia led to the decrease of cognitive ability. The blood concentrations of CD163 and TNF-α increased significantly at 24 h after the operation with sevoflurane anesthesia (P<0.05). Fluorescence microscopic observation showed that M2 was the main type of macrophages in normal tissues, while M1 and M2 phenotypes were highly expressed in sevoflurane anesthetized tissues at the same time, especially in M1 phenotypes (P<0.01). The polarization of macrophages in the anesthetic group showed the high level of M1 mRNA, and the expression levels of TNF-α, monocyte chemotactic protein 1(MCP-1) and Interleukin-6 (IL-6)mRNA in the anesthetic group were significantly higher than those in the control group (P<0.05). The expression levels of M2 mRNA such as transforming growth factor-β (TGF-β) and IL-10 were significantly lower than those in the control group (P<0.05). Compared with the control group, the expression of FoxO1 and p21 protein in the anesthesia group was significantly lower than that in the control group with a significant statistical difference (P<0.01). Conclusion: This study offers a theoretical basis and insight for further understanding of the prevention and treatment of cognitive dysfunction induced by anesthetic drugs.

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Wu, Ai-Luen, Jeong-Ho Kim, Chongben Zhang, Terry G. Unterman, and Jie Chen. "Forkhead Box Protein O1 Negatively Regulates Skeletal Myocyte Differentiation through Degradation of Mammalian Target of Rapamycin Pathway Components." Endocrinology 149, no. 3 (December 13, 2007): 1407–14. http://dx.doi.org/10.1210/en.2007-1470.

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The forkhead transcription factor forkhead box protein O1 (FoxO1), a downstream target of phosphatidylinositol 3-kinase/Akt signaling, has been reported to suppress skeletal myocyte differentiation, but the mechanism by which FoxO1 regulates myogenesis is not fully understood. We have previously demonstrated that a nutrient-sensing mammalian target of rapamycin (mTOR) pathway controls the autocrine production of IGF-II and the subsequent phosphatidylinositol 3-kinase/Akt signaling downstream of IGF-II in myogenesis. Here we report a regulatory loop connecting FoxO1 to the mTOR pathway. Inducible activation of a FoxO1 active mutant in the C2C12 mouse myoblasts blocks myogenic differentiation at an early stage and meanwhile leads to proteasome-dependent degradation of a specific subset of components in the mTOR signaling network, including mTOR, raptor, tuberous sclerosis complex 2, and S6 protein kinase 1. This function of FoxO1 requires new protein synthesis, consistent with the idea that a transcriptional target of FoxO1 may be responsible for the degradation of mTOR. We further show that active FoxO1 inhibits IGF-II expression at the transcriptional activation level, through the modulation of mTOR protein levels. Moreover, the addition of exogenous IGF-II fully rescues myocyte differentiation from FoxO inhibition. Taken together, we propose that the mTOR-IGF-II pathway is a major mediator of FoxO’s inhibitory function in skeletal myogenesis.

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Luo, Ying, Yan Lin, and Xiao Han. "Original article. Transcription factors regulate Forkhead box O1 gene promoter activity in pancreatic β-cells." Asian Biomedicine 5, no. 4 (August 1, 2011): 433–39. http://dx.doi.org/10.5372/1905-7415.0504.057.

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Abstract Background: Transcription factors of the Forkhead box O (Fox O) family have important roles in cellular proliferation, apoptosis, differentiation, and stress resistance. In pancreatic β-cells, FoxO1 protein plays an important role in β-cells development. The molecular mechanism of transcriptional regulation of basal FoxO1 gene expression in pancreatic β-cells is not fully understood. Objectives: Explore the potential transcription factors regulating FoxO1 promoter activity using pancreatic β-cell line (RINm5F cells) Methods: Promoter screening method, luciferase reporter gene analysis, transient expression assay system, and deletion analysis of a -974/-18 bp 5’ upstream region of the mouse FoxO1 gene were used in this study. Results: An inhibition domain (-974/-321) and an activation domain (-321/-18) was identified through deletion analysis of a -974/-18 bp 5’ upstream region of the mouse FoxO1 gene. Using the promoter screening method, several transcription factors were selected. Luciferase reporter studies showed that these factors could regulate FoxO1 promoter activity in RINm5F cells. Among these factors, cAMP response-element binding protein (CREB) could positively regulate FoxO1 promoter activity. Signal transducer and activator of transcription 1 (STAT1) played a negative role on FoxO1 promoter. In addition, ETS oncogene family member Elk-1 did not affect the FoxO1 promoter activity. Conclusion: Two transcription factors (CREB and STAT1) could effectively regulate the mouse FoxO1 gene promoter activity.

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Schroeder, Jennifer K., Cherie A. Kessler, and Stuart Handwerger. "Critical Role for TWIST1 in the Induction of Human Uterine Decidualization." Endocrinology 152, no. 11 (September 13, 2011): 4368–76. http://dx.doi.org/10.1210/en.2011-1140.

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The importance of the transcription factor TWIST1 for uterine decidualization was examined in human uterine fibroblast (HUF) cells decidualized in vitro with medroxyprogesterone, estradiol (E2), and prostaglandin E2. TWIST1 mRNA levels increased by 6.0- to 6.8-fold during the first 1–2 d of decidualization and remained above predecidualization levels for up to 15 d. Pretreatment of HUF cells with a TWIST1 small interfering RNA (siRNA) for 3 d before the induction of decidualization resulted in less morphologic differentiation than HUF cells pretreated with a nonsilencing control RNA. In addition, the cells pretreated with TWIST1 siRNA expressed 75–95% less IGF binding protein 1, LEFTY2, fibromodulin, laminin, and several other mRNA during decidualization, including the mRNA for the transcription factors forkhead box protein O1 and v-ets-erythroblastosis virus E26, both of which were previously shown to be critical for the induction of decidualization. The HUF cells pretreated with the TWIST1 siRNA also underwent less apoptosis during decidualization than the control cells, as evidenced by a 20% decrease in DNA fragmentation (terminal deoxynucleotidyl transferase 2′-deoxyuridine, 5′-triphosphate nick end labeling assay) and a 43–48% decrease in caspase 3, BCL2-associated X protein, and TNF receptor superfamily member 6 mRNA levels. Although the knockdown of TWIST1 expression markedly attenuated the induction of decidualization, overexpression of TWIST1 alone was insufficient to induce the decidualization of HUF cells. Taken together, these findings strongly implicate an essential role for TWIST1 in the initiation of human decidualization and uterine stromal cell apoptosis that occurs upstream of the induction of forkhead box protein O1 and v-ets-erythroblastosis virus E26 mRNA.

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Zhang, Hongxing, Xiaojuan Sun, and Dingjun Hao. "Upregulation of microRNA-370 facilitates the repair of amputated fingers through targeting forkhead box protein O1." Experimental Biology and Medicine 241, no. 3 (August 27, 2015): 282–89. http://dx.doi.org/10.1177/1535370215600549.

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Shimba, Yuki, Rena Senda, Keigo Katayama, Akihito Morita, Masahiko Ikeda, Yasutomi Kamei, and Shinji Miura. "Skeletal muscle-specific forkhead box protein-O1 overexpression suppresses atherosclerosis progression in apolipoprotein E-knockout mice." Biochemical and Biophysical Research Communications 540 (February 2021): 61–66. http://dx.doi.org/10.1016/j.bbrc.2021.01.001.

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Zhang, Shurun, Xiaoling Chen, Zhiqing Huang, Daiwen Chen, Bing Yu, Hong Chen, Junqiu Luo, Jun He, Ping Zheng, and Jie Yu. "Leucine promotes differentiation of porcine myoblasts through the protein kinase B (Akt)/Forkhead box O1 signalling pathway." British Journal of Nutrition 119, no. 7 (March 23, 2018): 727–33. http://dx.doi.org/10.1017/s0007114518000181.

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AbstractLeucine, one of the branched-chain amino acids, is the only amino acid to regulate protein turnover in skeletal muscle. Leucine not only increases muscle protein synthesis, but also decreases muscle protein degradation. It is well documented that leucine plays a positive role in differentiation of murine muscle cells. However, the role of leucine on porcine myoblast differentiation and its mechanism remains unclear. In this study, porcine myoblasts were induced to differentiate with differentiation medium containing different concentrations of leucine, and wortmannin was used to interdict the activity of protein kinase B (Akt). We found that leucine increased the number of myosin heavy chain-positive cells and creatine kinase activity. Moreover, leucine increased the mRNA and protein levels of myogenin and myogenic determining factor (MyoD). In addition, leucine increased the levels of phosphorylated Akt/Akt and phosphorylated Forkhead box O1 (P-FoxO1)/FoxO1, as well as decreased the protein level of FoxO1. However, wortmannin, a specific repressor of PI3K/Akt signalling pathway, attenuated the positive role of leucine on porcine myoblast differentiation. Our results suggest that leucine promotes porcine myoblast differentiation through the Akt/FoxO1 signalling pathway.

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Weeks, Kate, Helen Kiriazis, Yow Keat Tham, Bianca Bernardo, Nelly Cemerlang, and Julie McMullen. "Forkhead box protein O1 (FoxO1) is required for exercise-induced, but not PI3K-induced, physiological cardiac hypertrophy." Journal of Molecular and Cellular Cardiology 124 (November 2018): 93. http://dx.doi.org/10.1016/j.yjmcc.2018.07.037.

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Shi, Chun, Rongjie SHI, and Han Guo. "Tumor necrosis factor α reduces gonadotropin-releasing hormone release through increase of forkhead box protein O1 activity." NeuroReport 31, no. 6 (April 2020): 473–77. http://dx.doi.org/10.1097/wnr.0000000000001424.

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Takamura, Haruna, Kaya Yoshida, Hirohiko Okamura, Natsumi Fujiwara, and Kazumi Ozaki. "Porphyromonas gingivalis attenuates the insulin-induced phosphorylation and translocation of forkhead box protein O1 in human hepatocytes." Archives of Oral Biology 69 (September 2016): 19–24. http://dx.doi.org/10.1016/j.archoralbio.2016.05.010.

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Schimpl, Marianne, Alexander W. Schüttelkopf, Vladimir S. Borodkin, and Daan M. F. van Aalten. "Human OGA binds substrates in a conserved peptide recognition groove." Biochemical Journal 432, no. 1 (October 25, 2010): 1–12. http://dx.doi.org/10.1042/bj20101338.

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Modification of cellular proteins with O-GlcNAc (O-linked N-acetylglucosamine) competes with protein phosphorylation and regulates a plethora of cellular processes. O-GlcNAcylation is orchestrated by two opposing enzymes, O-GlcNAc transferase and OGA (O-GlcNAcase or β-N-acetylglucosaminidase), which recognize their target proteins via as yet unidentified mechanisms. In the present study, we uncovered the first insights into the mechanism of substrate recognition by human OGA. The structure of a novel bacterial OGA orthologue reveals a putative substrate-binding groove, conserved in metazoan OGAs. Guided by this structure, conserved amino acids lining this groove in human OGA were mutated and the activity on three different substrate proteins [TAB1 (transforming growth factor-β-activated protein kinase 1-binding protein 1), FoxO1 (forkhead box O1) and CREB (cAMP-response-element-binding protein)] was tested in an in vitro deglycosylation assay. The results provide the first evidence that human OGA may possess a substrate-recognition mechanism that involves interactions with O-GlcNAcylated proteins beyond the GlcNAc-binding site, with possible implications for differential regulation of cycling of O-GlcNAc on different proteins.

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Silveira, W. A., D. A. Gonçalves, F. A. Graça, A. L. Andrade-Lopes, L. B. Bergantin, N. M. Zanon, R. O. Godinho, I. C. Kettelhut, and L. C. C. Navegantes. "Activating cAMP/PKA signaling in skeletal muscle suppresses the ubiquitin-proteasome-dependent proteolysis: implications for sympathetic regulation." Journal of Applied Physiology 117, no. 1 (July 1, 2014): 11–19. http://dx.doi.org/10.1152/japplphysiol.01055.2013.

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Although we have recently demonstrated that plasma catecholamines induce antiproteolytic effects on skeletal muscle (Graça FA, Gonçalves DAP, Silveira WA, Lira EC, Chaves VE, Zanon NM, Garófalo MAR, Kettelhut IC, Navegantes LCC. Am J Physiol Endocrinol Metab. 305: E1483-E1494, 2013), the role of the muscle sympathetic innervation and, more specifically, norepinephrine (NE) in regulating the ubiquitin (Ub)-proteasome system (UPS) remains unknown. Based on previous findings that chemical sympathectomy acutely reduces UPS activity, we hypothesized that muscle NE depletion induces adrenergic supersensitivity in rat skeletal muscles. We report that surgical sympathetic denervation (SDEN), a condition in which only muscle NE from both hindlimbs is depleted, transiently reduced the overall proteolysis and the UPS activity (∼25%) in both soleus and extensor digitorum longus muscles. This antiproteolytic response was accompanied by increased activity of adenylyl cyclase (112%), levels of cyclic adenosine monophosphate (cAMP; 191%), and the serine phosphorylation of cAMP response element-binding protein (32%). In extensor digitorum longus from normal rats, NE (10−4M) in vitro increased the levels of cAMP (115%) and the serine phosphorylation of both cAMP response element-binding protein (2.7-fold) and forkhead box class O1 transcription factor. Similar effects were observed in C2C12cells incubated with forskolin (10 μM). In parallel, NE significantly reduced the basal UPS (21%) activity and the mRNA levels of atrophy-related Ub-ligases. Similar responses were observed in isolated muscles exposed to 6-BNZ-cAMP (500 μM), a specific PKA activator. The phosphorylation levels of Akt were not altered by SDEN, NE, forskolin or 6-BNZ-cAMP. Our results demonstrate that SDEN induces muscle adrenergic supersensitivity for cAMP leading to the suppression of UPS, and that the suppressive effects of NE on UPS activity and expression of Ub-ligases can be mediated by the activation of cAMP/PKA signaling, with the inhibition of forkhead box class O1 transcription factor.

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Said, Hebatallah, Manal L. Louka, Mariam Sameh, and Inas Mohamed Sabry. "Evaluation of nephroblastoma overexpressed gene, a transcriptional target of forkhead box protein O1 in type 2 diabetes mellitus." Meta Gene 12 (June 2017): 62–67. http://dx.doi.org/10.1016/j.mgene.2017.01.006.

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Tinkum, Kelsey L., Lynn S. White, Luciano Marpegan, Erik Herzog, David Piwnica-Worms, and Helen Piwnica-Worms. "Forkhead Box O1 (FOXO1) Protein, but Not p53, Contributes to Robust Induction of p21 Expression in Fasted Mice." Journal of Biological Chemistry 288, no. 39 (August 5, 2013): 27999–8008. http://dx.doi.org/10.1074/jbc.m113.494328.

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Fjällström, Ann-Kristin, Kim Evertsson, Marlene Norrby, and Sven Tågerud. "Forkhead box O1 and muscle RING finger 1 protein expression in atrophic and hypertrophic denervated mouse skeletal muscle." Journal of Molecular Signaling 9 (September 24, 2014): 9. http://dx.doi.org/10.1186/1750-2187-9-9.

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Chay, Doo Byung, Gwan Hee Han, Sanghee Nam, Hanbyoul Cho, Joon-Yong Chung, and Stephen M. Hewitt. "Forkhead box protein O1 (FOXO1) and paired box gene 3 (PAX3) overexpression is associated with poor prognosis in patients with cervical cancer." International Journal of Clinical Oncology 24, no. 11 (July 13, 2019): 1429–39. http://dx.doi.org/10.1007/s10147-019-01507-w.

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Zhang, Kebin, Xiaoqin Guo, Hui Yan, Yuxin Wu, Quan Pan, James Zheng Shen, Xiaopeng Li, et al. "Phosphorylation of Forkhead Protein FoxO1 at S253 Regulates Glucose Homeostasis in Mice." Endocrinology 160, no. 5 (April 5, 2019): 1333–47. http://dx.doi.org/10.1210/en.2018-00853.

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Abstract The transcription factor forkhead box O1 (FoxO1) is a key mediator in the insulin signaling pathway and controls multiple physiological functions, including hepatic glucose production (HGP) and pancreatic β-cell function. We previously demonstrated that S256 in human FOXO1 (FOXO1-S256), equivalent to S253 in mouse FoxO1 (FoxO1-S253), is a key phosphorylation site mediating the effect of insulin as a target of protein kinase B on suppression of FOXO1 activity and expression of target genes responsible for gluconeogenesis. Here, we investigated the role of FoxO1-S253 phosphorylation in control of glucose homeostasis in vivo by generating global FoxO1-S253A/A knockin mice, in which FoxO1-S253 alleles were replaced with alanine (A substitution) blocking FoxO1-S253 phosphorylation. FoxO1-S253A/A mice displayed mild increases in feeding blood glucose and insulin levels but decreases in fasting blood glucose and glucagon concentrations, as well as a reduction in the ratio of pancreatic α-cells/β-cells per islet. FoxO1-S253A/A mice exhibited a slight increase in energy expenditure but barely altered food intake and glucose uptake among tissues. Further analyses revealed that FoxO1-S253A/A enhances FoxO1 nuclear localization and promotes the effect of glucagon on HGP. We conclude that dephosphorylation of S253 in FoxO1 may reflect a molecular basis of pancreatic plasticity during the development of insulin resistance.

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Sun, Zhihua, Peiyi Li, Xiao Wang, Shuchang Lai, Hong Qiu, Zhi Chen, Shidi Hu, Jie Yao, and Jie Shen. "GLP-1/GLP-1R Signaling Regulates Ovarian PCOS-Associated Granulosa Cells Proliferation and Antiapoptosis by Modification of Forkhead Box Protein O1 Phosphorylation Sites." International Journal of Endocrinology 2020 (June 19, 2020): 1–10. http://dx.doi.org/10.1155/2020/1484321.

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As the major cause of female anovulatory infertility, polycystic ovary syndrome (PCOS) affects a great proportion of women at childbearing age. Although glucagon-like peptide 1 receptor agonists (GLP-IRAs) show therapeutic effects for PCOS, its target and underlying mechanism remains elusive. In the present study, we identified that, both in vivo and in vitro, GLP-1 functioned as the regulator of proliferation and antiapoptosis of MGCs of follicle in PCOS mouse ovary. Furthermore, forkhead box protein O1 (FoxO1) plays an important role in the courses. Regarding the importance of granulosa cells (GCs) in oocyte development and function, the results from the current study could provide a more detailed illustration on the already known beneficial effects of GLP-1RAs on PCOS and support the future efforts to develop more efficient GLP-1RAs for PCOS treatment.

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El Ouaamari, Abdelfattah, InSug O-Sullivan, Jun Shirakawa, Giorgio Basile, Wenwei Zhang, Sandra Roger, Thomas Thomou, et al. "Forkhead box protein O1 (FoxO1) regulates hepatic serine protease inhibitor B1 (serpinB1) expression in a non-cell-autonomous fashion." Journal of Biological Chemistry 294, no. 3 (November 20, 2018): 1059–69. http://dx.doi.org/10.1074/jbc.ra118.006031.

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Wei, Rongxue, Chunchun Han, Fang He, Xiangping Xiong, Fengjiang Ye, Hehe Liu, Liang Li, Hongyong Xu, Shouhai Wei, and Xianyin Zeng. "Role of forkhead box protein O1 and insulin on cell proliferation mediated by sirtuin 1 in goose primary hepatocytes." Journal of Applied Poultry Research 30, no. 2 (June 2021): 100144. http://dx.doi.org/10.1016/j.japr.2021.100144.

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Lee, Hyejin, Ji Hye Jeong, and Jae-Ha Ryu. "Lignan from Alnus japonica Inhibits Adipocyte Differentiation via Cell Cycle and FOXO1 Regulation." Molecules 25, no. 15 (July 23, 2020): 3346. http://dx.doi.org/10.3390/molecules25153346.

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In the present study, we isolated a lignan ((−)-(2R,3R)-1,4-O-diferuloylsecoisolariciresinol, DFS) from Alnus japonica and evaluated its antiobesity potential in vitro. We also determined its mechanism of action in a mouse pre-adipocyte 3T3-L1 cell line. DFS dose- and day-dependently inhibited adipogenesis by downregulation of adipogenic factors and lipid metabolism-regulating factors during adipocyte differentiation. In particular, DFS suppressed cell cycle-regulating factors and induced G0/G1 cell cycle arrest, implying that it had an inhibitory effect on mitotic clonal expansion which occurred at an early stage of adipogenesis. DFS also suppressed adipogenesis through decreasing Akt phosphorylation and increasing the level of Forkhead box protein-O1 (FOXO1). These results suggest that DFS may be a pharmacological candidate for the development of antiobesity, therapeutic, and nutraceutical products.

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Teot, Lisa A., Michaela Schneider, Aaron R. Thorner, Jing Tian, Yueh-Yun Chi, Matthew Ducar, Ling Lin, et al. "Clinical and mutational spectrum of highly differentiated, paired box 3:forkhead box protein o1 fusion-negative rhabdomyosarcoma: A report from the Children's Oncology Group." Cancer 124, no. 9 (February 20, 2018): 1973–81. http://dx.doi.org/10.1002/cncr.31286.

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Qiu, Yueqin, Kebiao Li, Xichen Zhao, Shilong Liu, Li Wang, Xuefen Yang, and Zongyong Jiang. "Fermented Feed Modulates Meat Quality and Promotes the Growth of Longissimus Thoracis of Late-Finishing Pigs." Animals 10, no. 9 (September 17, 2020): 1682. http://dx.doi.org/10.3390/ani10091682.

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This study investigated the effect of fermented diet on growth performance, carcass traits, meat quality and growth of longissimus thoracis (LT) of finishing pigs. A total of 48 finishing pigs [Duroc × (Landrace × Large White), male, 126 ± 5-d-old] weighing 98.76 ± 1.27 kg were randomly assigned to two treatments (eight pens per treatment and three pigs per pen) for a 28-d feeding trial, including control diet and fermented diet. Fermented diet significantly increased the loin eye area and lean mass percentage, decreased backfat thickness and improved meat quality of LT by decreasing the shear force and drip loss at 48 h post slaughter and improving meat sensory characteristics compared with control diet. A fermented diet also significantly increased the abundance of insulin, insulin receptor (IR), myoblast determination protein (MyoD) and myosin heavy chain-I (MyHC-I) transcripts, and the phosphorylation levels of AKT, mTORC1, 4EBP1 and S6K1 in LT, while decreasing the expression of muscle atrophy F-box (MAFbx) and forkhead Box O1 (Foxo1) mRNA transcripts. Moreover, proteomic analysis revealed that differentially expressed proteins predominantly involved in protein synthesis and muscle development were modulated by fermented diet. Our results indicated that a fermented diet improved meat quality and enhanced LT growth of finishing pigs by increasing insulin/AKT/mTORC1 protein synthesis cascade and activating the Foxo1/MAFbx pathway, along with the regulation of ribosomal protein and proteins involved in muscle contraction and muscle hypertrophy.

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Park, Jae-Yeo, Younghwa Kim, Jee Ae Im, Seungkwon You, and Hyangkyu Lee. "Inhibition of Adipogenesis by Oligonol through Akt-mTOR Inhibition in 3T3-L1 Adipocytes." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/895272.

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Polyphenols have recently become an important focus of study in obesity research. Oligonol is an oligomerized polyphenol, typically comprised of catechin-type polyphenols from a variety of fruits, which has been found to exhibit better bioavailability and bioreactivity than natural polyphenol compounds. Here, we demonstrated that Oligonol inhibits 3T3-L1 adipocyte differentiation by reducing adipogenic gene expression. During adipogenesis, Oligonol downregulated the mRNA levels of peroxisome proliferator-activated receptorγ(PPARγ), CCAAT/enhancer binding proteins α (C/EBPα), andδ(C/EBPδ) in a dose-dependent manner and the expression of genes involved in lipid biosynthesis. The antiadipogenic effect of Oligonol appears to originate from its ability to inhibit the Akt and mammalian target of rapamycin (mTOR) signaling pathway by diminishing the phosphorylation of ribosomal protein S6 kinase (p70S6K), a downstream target of mTOR and forkhead box protein O1 (Foxo1). These results suggest that Oligonol may be a potent regulator of obesity by repressing major adipogenic genes through inhibition of the Akt signaling pathway, which induces the inhibition of lipid accumulation, ultimately inhibiting adipogenesis.

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Sumi, Koichiro, Kinya Ashida, and Koichi Nakazato. "Resistance exercise with anti-inflammatory foods attenuates skeletal muscle atrophy induced by chronic inflammation." Journal of Applied Physiology 128, no. 1 (January 1, 2020): 197–211. http://dx.doi.org/10.1152/japplphysiol.00585.2019.

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Chronic inflammation (CI) can contribute to muscle atrophy and sarcopenia. Resistance exercise (RE) promotes increased and/or maintenance of skeletal muscle mass, but the effects of RE in the presence of CI are unclear. In this study, we developed a novel animal model of CI-induced muscle atrophy and examined the effect of acute or chronic RE by electrical stimulation. CI was induced in young female Lewis rats by injection with peptidoglycan-polysaccharide (PG-PS). Extracellular signal-regulated kinase (ERK), p70S6 kinase (p70S6K), 4E binding protein 1 (4E-BP1), Akt, and Forkhead box O1 (FOXO1) phosphorylation levels increased in gastrocnemius (Gas) muscle from normal rats subjected to acute RE. After acute RE in CI rats, increased levels of phosphorylated ERK, p70S6K, and 4E-BP1, but not Akt or FOXO1, were observed. Chronic RE significantly increased the Gas weight in the exercised limb relative to the nontrained opposing limb in CI rats. Dietary supplementation with anti-inflammatory agents, eicosapentaenoic/docosahexaenoic acid and α-lactalbumin attenuated CI-induced muscle atrophy in the untrained Gas and could promote RE-induced inhibition of atrophy in the trained Gas. In the trained leg, significant negative correlations ( r ≤ −0.80) were seen between Gas weights and CI indices, including proinflammatory cytokines and white blood cell count. These results indicated that the anabolic effects of RE are effective for preventing CI-induced muscle atrophy but are partially attenuated by inflammatory molecules. The findings also suggested that anti-inflammatory treatment together with RE is an effective intervention for muscle atrophy induced by CI. Taken together, we conclude that systemic inflammation levels are associated with skeletal muscle protein metabolism and plasticity. NEW & NOTEWORTHY This study developed a novel chronic inflammation (CI) model rat demonstrating that resistance exercise (RE) induced activation of protein synthesis signaling pathways and mitigated skeletal muscle atrophy. These anabolic effects were partially abrogated likely through attenuation of Akt/Forkhead box O1 axis activity. The degree of skeletal muscle atrophy was related to inflammatory responses. Dietary supplementation with anti-inflammatory agents could enhance the anabolic effect of RE. Our findings provide insight for development of countermeasures for CI-related muscle atrophy, especially secondary sarcopenia.

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Ujvari, Dorina, Ivika Jakson, Shabnam Babayeva, Daniel Salamon, Bence Rethi, Sebastian Gidlöf, and Angelica Lindén Hirschberg. "Dysregulation of In Vitro Decidualization of Human Endometrial Stromal Cells by Insulin via Transcriptional Inhibition of Forkhead Box Protein O1." PLOS ONE 12, no. 1 (January 30, 2017): e0171004. http://dx.doi.org/10.1371/journal.pone.0171004.

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Heidari, Laleh, Sayyed Mohammad Hossein Ghaderian, Hossein Vakili, and Tayyeb Ali Salmani. "Promoter methylation and functional variants in arachidonate 5‐lipoxygenase and forkhead box protein O1 genes associated with coronary artery disease." Journal of Cellular Biochemistry 120, no. 8 (March 2019): 12360–68. http://dx.doi.org/10.1002/jcb.28501.

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Peng, Shiming, Wen Xiao, Dapeng Ju, Baofa Sun, Nannan Hou, Qianlan Liu, Yanli Wang, et al. "Identification of entacapone as a chemical inhibitor of FTO mediating metabolic regulation through FOXO1." Science Translational Medicine 11, no. 488 (April 17, 2019): eaau7116. http://dx.doi.org/10.1126/scitranslmed.aau7116.

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Recent studies have established the involvement of the fat mass and obesity-associated gene (FTO) in metabolic disorders such as obesity and diabetes. However, the precise molecular mechanism by which FTO regulates metabolism remains unknown. Here, we used a structure-based virtual screening of U.S. Food and Drug Administration–approved drugs to identify entacapone as a potential FTO inhibitor. Using structural and biochemical studies, we showed that entacapone directly bound to FTO and inhibited FTO activity in vitro. Furthermore, entacapone administration reduced body weight and lowered fasting blood glucose concentrations in diet-induced obese mice. We identified the transcription factor forkhead box protein O1 (FOXO1) mRNA as a direct substrate of FTO, and demonstrated that entacapone elicited its effects on gluconeogenesis in the liver and thermogenesis in adipose tissues in mice by acting on an FTO-FOXO1 regulatory axis.

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Lin, Yu-Min, Hung-Yu Sun, Wen-Tai Chiu, Hui-Chen Su, Yu-Chieh Chien, Heng-Ai Chang, Lee-Won Chong, et al. "Etifoxine, a TSPO Ligand, Worsens Hepatitis C-Related Insulin Resistance but Relieves Lipid Accumulation." BioMed Research International 2019 (March 11, 2019): 1–11. http://dx.doi.org/10.1155/2019/3102414.

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Etifoxine, an 18 kDa translocator protein (TSPO) agonist for the treatment of anxiety disorders in clinic, may be able to cause acute liver injury or cytolytic hepatitis. TSPO has been demonstrated to participate in inflammatory responses in infective diseases as well as to modulate glucose and lipid homeostasis. Hepatitis C virus (HCV) infection disrupts glucose and lipid homoeostasis, leading to insulin resistance (IR). Whether TSPO affects the HCV-induced IR remains unclear. Here, we found that the administration of etifoxine increased the TSPO protein expression and recovered the HCV-mediated lower mitochondrial membrane potential (MMP) without affecting HCV infection. Moreover, etifoxine reversed the HCV-induced lipid accumulation by modulating the expressions of sterol regulatory element-binding protein-1 and apolipoprotein J. On the other hand, in infected cells pretreated with etifoxine, the insulin-mediated insulin receptor substrate-1/Akt signals, forkhead box protein O1 translocation, and glucose uptake were blocked. Taken together, our results pointed out that etifoxine relieved the HCV-retarded MMP and reduced the lipid accumulation but deteriorated the HCV-induced IR by interfering with insulin signal molecules.

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GAO, FENG, and WENHUI WANG. "MicroRNA-96 promotes the proliferation of colorectal cancer cells and targets tumor protein p53 inducible nuclear protein 1, forkhead box protein O1 (FOXO1) and FOXO3a." Molecular Medicine Reports 11, no. 2 (November 4, 2014): 1200–1206. http://dx.doi.org/10.3892/mmr.2014.2854.

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Dou, Ce, Nan Li, Ning Ding, Chuan Liu, Xiaochao Yang, Fei Kang, Zhen Cao, et al. "HDAC2 regulates FoxO1 during RANKL-induced osteoclastogenesis." American Journal of Physiology-Cell Physiology 310, no. 10 (May 15, 2016): C780—C787. http://dx.doi.org/10.1152/ajpcell.00351.2015.

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The bone-resorbing osteoclast (OC) is essential for bone homeostasis, yet deregulation of OCs contributes to diseases such as osteoporosis, osteopetrosis, and rheumatoid arthritis. Here we show that histone deacetylase 2 (HDAC2) is a key positive regulator during receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis and bone resorption. Bone marrow macrophages (BMMs) showed increased HDAC2 expression during osteoclastogenesis. HDAC2 overexpression enhanced, whereas HDAC2 deletion suppressed osteoclastogenesis and bone resorption using lentivirus infection. Mechanistically, upon RANKL activation, HDAC2 activated Akt; Akt directly phosphorylates and abrogates Forkhead box protein O1 (FoxO1), which is a negative regulator during osteoclastogenesis through reducing reactive oxygen species. HDAC2 deletion in BMMs resulted in decreased Akt activation and increased FoxO1 activity during osteoclastogenesis. In conclusion, HDAC2 activates Akt thus suppresses FoxO1 transcription results in enhanced osteoclastogenesis. Our data imply the potential value of HDAC2 as a new target in regulating osteoclast differentiation and function.

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Ren, Liang, Jing Yang, Jun Wang, Xuedong Zhou, and Chengcheng Liu. "The Roles of FOXO1 in Periodontal Homeostasis and Disease." Journal of Immunology Research 2021 (March 30, 2021): 1–12. http://dx.doi.org/10.1155/2021/5557095.

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Periodontitis is an oral chronic inflammatory disease that is initiated by periodontal microbial communities and requires disruption of the homeostatic responses. The prevalence of periodontal disease increases with age; more than 70% of adults 65 years and older have periodontal disease. A pathogenic microbial community is required for initiating periodontal disease. Dysbiotic immune-inflammatory response and bone remodeling are characteristics of periodontitis. The transcription factor forkhead box protein O1 (FOXO1) is a key regulator of a number of cellular processes, including cell survival and differentiation, immune status, reactive oxygen species (ROS) scavenging, and apoptosis. Although accumulating evidence indicates that FOXO1 activity can be induced by periodontal pathogens, the roles of FOXO1 in periodontal homeostasis and disease have not been well documented. The present review summarizes how the FOXO1 signaling axis can regulate periodontal bacteria-epithelial interactions, immune-inflammatory response, bone remodeling, and wound healing.

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Zhang, B., L. Gui, L. Zhu, X. Zhao, Y. Yang, and Q. Li. "Forkhead box protein O1 mediates apoptosis in a cancer cervical cell line treated with the antitumor agent tumor necrosis factor-α." Genetics and Molecular Research 14, no. 3 (2015): 7446–54. http://dx.doi.org/10.4238/2015.july.3.20.

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Garcia Whitlock, Anna E., Matthew Gavin, Carrie A. Sims, and Paul M. Titchenell. "Inhibition of the Liver Insulin Responsive Transcription Factor Forkhead Box Protein O1 Fails to Rescue Stress Hyperglycemia in Trauma and Hemorrhage." Journal of the American College of Surgeons 229, no. 4 (October 2019): S299—S300. http://dx.doi.org/10.1016/j.jamcollsurg.2019.08.656.

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Bai, Xiaoyan, Jian Geng, Xiao Li, Jiao Wan, Jixing Liu, Zhanmei Zhou, and Xiaoting Liu. "Long Noncoding RNA LINC01619 Regulates MicroRNA-27a/Forkhead Box Protein O1 and Endoplasmic Reticulum Stress-Mediated Podocyte Injury in Diabetic Nephropathy." Antioxidants & Redox Signaling 29, no. 4 (August 2018): 355–76. http://dx.doi.org/10.1089/ars.2017.7278.

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Bär, Ludmilla, Martina Feger, Abul Fajol, Lars-Oliver Klotz, Shufei Zeng, Florian Lang, Berthold Hocher, and Michael Föller. "Insulin suppresses the production of fibroblast growth factor 23 (FGF23)." Proceedings of the National Academy of Sciences 115, no. 22 (May 14, 2018): 5804–9. http://dx.doi.org/10.1073/pnas.1800160115.

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Fibroblast growth factor 23 (FGF23) is produced by bone cells and regulates renal phosphate and vitamin D metabolism, as well as causing left ventricular hypertrophy. FGF23 deficiency results in rapid aging, whereas high plasma FGF23 levels are found in several disorders, including kidney or cardiovascular diseases. Regulators of FGF23 production include parathyroid hormone (PTH), calcitriol, dietary phosphate, and inflammation. We report that insulin and insulin-like growth factor 1 (IGF1) are negative regulators of FGF23 production. In UMR106 osteoblast-like cells, insulin and IGF1 down-regulated FGF23 production by inhibiting the transcription factor forkhead box protein O1 (FOXO1) through phosphoinositide 3-kinase (PI3K)/protein kinase B (PKB)/Akt signaling. Insulin deficiency caused a surge in the serum FGF23 concentration in mice, which was reversed by administration of insulin. In women, a highly significant negative correlation between FGF23 plasma concentration and increase in plasma insulin level following an oral glucose load was found. Our results provide strong evidence that insulin/IGF1-dependent PI3K/PKB/Akt/FOXO1 signaling is a powerful suppressor of FGF23 production in vitro as well as in mice and in humans.

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Meister, Sabrina, Steffen E. Storck, Erik Hameister, Christian Behl, Sascha Weggen, Albrecht M. Clement, and Claus U. Pietrzik. "Expression of the ALS-Causing Variant hSOD1G93A Leads to an Impaired Integrity and Altered Regulation of Claudin-5 Expression in an in Vitro Blood–Spinal Cord Barrier Model." Journal of Cerebral Blood Flow & Metabolism 35, no. 7 (April 8, 2015): 1112–21. http://dx.doi.org/10.1038/jcbfm.2015.57.

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by progressive paralysis due to the loss of primary and secondary motor neurons. Mutations in the Cu/Zn-superoxide dismutase (SOD1) gene are associated with familial ALS and to date numerous hypotheses for ALS pathology exist including impairment of the blood–spinal cord barrier. In transgenic mice carrying mutated SOD1 genes, a disrupted blood–spinal cord barrier as well as decreased levels of tight junction (TJ) proteins ZO-1, occludin, and claudin-5 were detected. Here, we examined TJ protein levels and barrier function of primary blood–spinal cord barrier endothelial cells of presymptomatic hSOD1G93A mice and bEnd.3 cells stably expressing hSOD1G93A. In both cellular systems, we observed reduced claudin-5 levels and a decreased transendothelial resistance (TER) as well as an increased apparent permeability. Analysis of the β-catenin/AKT/forkhead box protein O1 (FoxO1) pathway and the FoxO1-regulated activity of the claudin-5 promoter revealed a repression of the claudin-5 gene expression in hSOD1G93A cells, which was depended on the phosphorylation status of FoxO1. These results strongly indicate that mutated SOD1 affects the expression and localization of TJ proteins leading to impaired integrity and breakdown of the blood–spinal cord barrier.

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Huang, Xiaojun, Huan Chen, Yunyi Xie, Zeyuan Cao, Xuefeng Lin, and Yan Wang. "FoxO1 Overexpression Ameliorates TNF-α-Induced Oxidative Damage and Promotes Osteogenesis of Human Periodontal Ligament Stem Cells via Antioxidant Defense Activation." Stem Cells International 2019 (October 31, 2019): 1–10. http://dx.doi.org/10.1155/2019/2120453.

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Periodontitis is a chronic disease that includes the pathologic loss of periodontal tissue and alveolar bone. The inflammatory environment in periodontitis impairs the osteogenic differentiation potential and depresses the regeneration capacity of human periodontal ligament stem cells (hPDLSCs). Since Forkhead box protein O1 (FoxO1) plays an important role in redox balance and bone formation, we investigated the role of FoxO1 in oxidative stress resistance and osteogenic differentiation in an inflammatory environment by overexpressing FoxO1 in hPDLSCs. First, we found that FoxO1 overexpression reduced reactive oxygen species (ROS) accumulation, decreased malondialdehyde (MDA) levels, and elevated antioxidant potential under oxidative condition. Next, the overexpression of FoxO1 protected hPDLSCs against oxidative damage, which involved stabilization of the mitochondrial membrane potential. Third, overexpressed FoxO1 promoted extracellular matrix (ECM) mineralization and increased the expression of the osteogenic markers Runx2 and SP7 in the inflammatory environment. These results indicated that FoxO1 overexpression in hPDLSCs has an anti-inflammatory effect, increases antioxidative capacity, and positively regulates osteogenesis in a mimicked inflammatory environment.

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Journal articles on the topic 'Forkhead Box Protein O1'

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