FOXO Transcriptional Factors and Long‐Term Living

Murtaza, Ghulam; Khan, Abida Kalsoom; Rashid, Rehana; Muneer, Saiqa; Hasan, Syed Muhammad Farid; Chen, Jianxin

doi:10.1155/2017/3494289

Cited by 133 publications

(101 citation statements)

References 102 publications

(123 reference statements)

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“…Hence, we found that up-regulation of TCF19 enhances the G1/S phase transition in HCC cells. Increasing studies have also established that FOXO1 is involved in diverse cellular pathways; including proliferation, stress resistance, differentiation and apoptosis [23]. Deregulation of FOXO1 has been found in many cancers, including prostate cancer, leukemia and melanoma [24][25][26].…”

Section: Discussionmentioning

confidence: 99%

TCF19 enhances cell proliferation in hepatocellular carcinoma by activating the ATK/FOXO1 signaling pathway

Zeng¹,

Feng²,

Zhao³

et al. 2019

neo

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Hepatocellular carcinoma (HCC) is one of the most lethal malignancies because of its complexity, high metastasis, recurrence and limited treatment options. Reports state that transcription factor 19 (TCF19) is related to the susceptibility to chronic HBV infection and that it strongly increases the risk of HCC occurrence, but its molecular mechanisms remain unknown. This study analyzed the datasets and confirmed that TCF19 is significantly increased in HCC cell lines and tissues. MTT and colony formation assay revealed that TCF19 over-expression enhances cell proliferation and tumorigenesis. Flow cytometry assay then determined that TCF over-expression helps HCC cell G1/S phase transition, and further research showed that TCF19 up-regulation inhibits p57 Kip2 , p21 Cip1 and p27 Kip1 cell cycle suppressors, enhances the expression of cyclin D1 expression and simulates retinoblastoma (Rb), FOXO1 and AKT phosphorylation. In addition, AKT and FOXO1 inhibitors suppress the TCF19 effect on cell proliferation. This demonstrates that AKT/FOXO1 signaling is essential for TCF19 influence on HCC progression, and our combined results suggest that crucial links between TCF19 and HCC can provide a novel target for hepatocellular carcinoma treatment.

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Section: Discussionmentioning

confidence: 99%

TCF19 enhances cell proliferation in hepatocellular carcinoma by activating the ATK/FOXO1 signaling pathway

Zeng¹,

Feng²,

Zhao³

et al. 2019

neo

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“…Numerous studies showed the transcription factor family, FOXO, impacts cell growth, proliferation, differentiation, and longevity (Murtaza et al, ). FOXO transcription factors act to integrate cellular signals of insulin, growth factors, cytokines, and oxidative stress (Klotz et al, ; Myatt, Brosens, & Lam, ; Tzivion et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies showed the transcription factor family, FOXO, impacts cell growth, proliferation, differentiation, and longevity (Murtaza et al, 2017). AKT, a serine/threonine-specific protein kinase that phosphorylate many of its downstream targets to regulate cell metabolism, also phosphorylates FOXO3α at Threonine 32, Serine 253, and Serine 315 residues (Tzivion et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

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Casticin prevents DSS induced ulcerative colitis in mice through inhibitions of NF‐κB pathway and ROS signaling

Yin

et al. 2018

Phytotherapy Research

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Casticin, a compound purified from the Chinese herb Viticis Fructus, has been proven effective in preventing tumor progression in previous studies. Ulcerative colitis (UC) is a common inflammatory bowel disease that affects millions of people worldwide, but no effective and safe drugs are available. In this study, we aimed to study how did casticin affect UC by evaluating its effects on dextran sulfate sodium (DSS)-induced colitis in mice. Our data suggested that casticin attenuated body weight loss, colon length shortening, and pathological damage in the colon of DSS-treated mice. Casticin decreased reactive oxygen species level and chemocytokines (IL-1β, IL-6, TNF-α) productions in colon tissue. The decreased reactive oxygen species level and suppressed proinflammatory cytokines productions were also confirmed in casticin-treated LPS-stimulated RAW264.7 cells and hydrogen peroxide-treated CACO-2 cells in vitro. Mechanistically, casticin treatment prevented the profound activation of AKT signaling caused by DSS administration. And casticin inhibited the productions of proinflammatory chemocytokines through downregulating AKT/NF-κB pathway in macrophages. Meanwhile, data revealed that casticin increased expressions of endogenous antioxidants peroxiredoxin 3 and MnSOD were through activation in FOXO3α signaling by downregulating AKT signaling in colon epithelium cells. Our findings demonstrated that casticin alleviated DSS-induced UC by increasing the antioxidant enzyme peroxiredoxin 3 and MnSOD expressions, and decreasing the production of proinflammatory chemocytokines through inhibition of AKT signaling.

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“…The forkhead box O (FOXO) transcription factors are critical players that modulate the expression of genes involved in growth, stress resistance, neurological diseases, cancer, and metabolism (Coomans de Brachene & Demoulin, ; Fluteau et al., ; Murtaza et al., ). Drosophila possesses one FOXO factor, whereas human has FOXO1,3,4, and 6, among which FOXO1 and FOXO3 are the main isoforms (Webb & Brunet, ).…”

Section: Introductionmentioning

confidence: 99%

eIF2α kinases PERK and GCN2 act on FOXO to potentiate FOXO activity

You

et al. 2018

Genes to Cells

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PERK and GCN2 are eIF2α kinases known to mediate the effects of ER stress and respond to an array of diverse stress stimuli. Previously, we reported that ER stress potentiates insulin resistance through PERK-mediated FOXO phosphorylation. Inhibition of PERK improves cellular insulin responsiveness at the level of FOXO activity. Here we provide further evidence that FOXO is required for the functional output of PERK by showing that lowering FOXO activity ameliorates a PERK gain-of-function phenotype in Drosophila. More importantly, we present results demonstrating that GCN2 acts similarly to PERK to promote FOXO activity. Regulation of FOXO by GCN2 is evolutionarily conserved and can be compensated for by PERK. The combination of these mechanisms may contribute to the complex regulatory network between PERK, GCN2, and FOXO, which has been implicated in the development and progression of a variety of diseases.

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FOXO Transcriptional Factors and Long‐Term Living

Cited by 133 publications

References 102 publications

TCF19 enhances cell proliferation in hepatocellular carcinoma by activating the ATK/FOXO1 signaling pathway

TCF19 enhances cell proliferation in hepatocellular carcinoma by activating the ATK/FOXO1 signaling pathway

Casticin prevents DSS induced ulcerative colitis in mice through inhibitions of NF‐κB pathway and ROS signaling

eIF2α kinases PERK and GCN2 act on FOXO to potentiate FOXO activity

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