p53-dependent growth arrest and induction of p21: A critical role for PCAF-mediated histone acetylation

Eckner, Richard

doi:10.4161/cc.21235

Cited by 20 publications

(17 citation statements)

References 9 publications

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“…21,28 Furthermore, P53, which targeting the P21, can induce the cell growth by blocking the cell cycle and the cell cycle would be arrested in G0-G1 phase when the P53-P21 signaling pathway is activated. [37][38][39][40] Our study found that the cell cycle was arrested at G0-G1 phase when YY1 was overexpressed in pancreatic cells, and CDKN3 overexpression notably facilitated the cell cycle into S phase through interacting with MdM2-P53 to downregulate the expression of P21 in pancreatic cancer cells. The decrease of P21 expression leads to cell cycle into S phase, which is DNA synthesis stage, and its proportion represents cell proliferation ability.…”

Section: Discussionmentioning

confidence: 61%

RETRACTED: YY1 suppresses proliferation and migration of pancreatic ductal adenocarcinoma by regulating the CDKN3/MdM2/P53/P21 signaling pathway

Liu

Zhang

et al. 2017

Intl Journal of Cancer

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Pancreatic ductal adenocarcinoma (PDAC) is one of the malignant lethal tumors. It has been reported that the transcriptional regulator Yin Yang-1 (YY1) suppressed the invasion and metastasis of PDAC. However, the function of YY1 on proliferation and migration of pancreatic cancer remains to be clarified. In this study, we found that YY1 overexpression or knockdown can inhibit or promote the proliferation and migration of pancreatic cancer cells. Digital gene expression sequencing indicates that cyclin-dependent kinase inhibitor 3 (CDKN3) may be the candidate target gene of YY1. Then we found that YY1 can downregulate the expression of CDKN3 by directly binding to the promoter region of CDKN3. Silencing CDKN3 expression could inhibit the ability of cell proliferation and migration and overexpression of CDKN3 could restore the effects induced by YY1 overexpression in pancreatic cancer cells. The expression levels of YY1 and CDKN3 were negatively correlated in pancreatic cancer tissues and PDAC patients with higher levels of CDKN3 have poor prognosis. Vitro and vivo study show that CDKN3 can form a complex with MdM2-P53, thus leading to inhibiting the expression of P21, which is the target gene of P53, and finally facilitates the cell cycle to promote the proliferation of pancreatic cancer cells. Hence, YY1 can directly regulate the expression of CDKN3 and participate in the cycle of pancreatic cancer cells, which can inhibit the progression of pancreatic cancer. These results reveal that YY1-CDKN3-MDM2/P53-P21 axis is involved in pancreatic tumorigenesis, which may develop new methods for human pancreatic cancer therapy.

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Section: Discussionmentioning

confidence: 61%

RETRACTED: YY1 suppresses proliferation and migration of pancreatic ductal adenocarcinoma by regulating the CDKN3/MdM2/P53/P21 signaling pathway

Liu

Zhang

et al. 2017

Intl Journal of Cancer

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“…p53, which targets p21, can inhibit cell growth by blocking the cell cycle and induction of cell cycle arrest in the G0-G1 phase when the p53-p21 signaling pathway is activated [25]. One study has reported the role of p21 in potentiating cancer stem cells via activation of canonical Wnt signaling due to TCF1/Cyclin D1 upregulation.…”

Section: Discussionmentioning

confidence: 99%

Polysaccharide from angelica sinensis attenuates SNP-Induced Apoptosis in osteoarthritis Chondrocytes by Inducing Autophagy via ERK1/2 Pathway

Zhuang

et al. 2020

Preprint

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Objective Chondrocyte apoptosis plays a vital role in osteoarthritis (OA) progression. Angelica sinensis polysaccharide (ASP), a traditional Chinese medicine, possesses anti-inflammatory and anti-apoptotic properties in chondrocytes. This study aimed to determine the protective role of ASP on sodium nitroprusside (SNP)-induced chondrocyte apoptosis, and explore the underlying mechanism. Method Human primary chondrocytes isolated from articular cartilage of OA patients were treated with SNP alone or in combination with different dose of ASP. Cell viability and apoptosis were assessed, and apoptosis-related proteins including Bcl-2 and Bax were detected. Autophagy levels were evaluated by light chain 3 (LC3)-II immunofluorescence staining, mRFP-GFP-LC3 fluorescence localisation and western blot (LC3II, p62, Beclin-1, Atg5). Meanwhile,activation of ERK 1/2 pathway was determined by western blot. The autophagy inhibitors 3-Methyladenine (3-MA), chloroquine (CQ) and a specific inhibitor of ERK1/2, SCH772984, were used respectively to confirm the autophagic effect of ASP. Results The results showed that SNP-induced chondrocyte apoptosis was significantly rescued by ASP, whereas ASP alone promoted chondrocytes proliferation. The anti-apoptotic effect of ASP was related to the enhanced autophagy and depended on the activation of ERK1/2 pathway.Conclusion ASP markedly rescued SNP-induced chondrocyte apoptosis by activating ERK1/2-dependent autophagy in chondrocytes, and it made ASP a potential therapeutic supplementation for OA treatment.

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“…Various oncogenes and tumor suppressors have been shown to be involved in the regulation of senescence-inducing pathways, and senescence induction appears to be an important step in the tumor regression [47]. The p53 / p21 and p16 / pRb tumor suppressor pathways are the most important regulators of cellular senescence and tumor progression [48]. Study showed that the two tumor suppressor pathways were putative targets for various cancer therapies because of their significant effect on senescence [49, 50].…”

Section: Discussionmentioning

confidence: 99%

lncRNA miat functions as a ceRNA to upregulate sirt1 by sponging miR-22-3p in HCC cellular senescence

Zhao

Cao

et al. 2019

Aging

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Hepatocellular carcinoma (HCC) is a leading cause of cancer related deaths and lacks effective therapies. Cellular senescence acts as a barrier against cancer progression and plays an important role in tumor suppression. Senescence associated long noncoding RNAs (SAL-RNAs) are thought to be critical regulators of cancer development. Here, the long noncoding RNA (lncRNA) myocardial infarction-associated transcript (miat) was first identified as an HCC specific SALncRNA. Knockdown of miat significantly promoted cellular senescence and inhibited HCC progression. Mechanistic study revealed that SAL-miat acted as a competitive endogenous RNA (ceRNA) that upregulated the expression of sirt1 by sponging miR-22-3p. Moreover, miat downregulation activated the tumor suppressor pathway (p53/p21 and p16/pRb) and stimulated senescent cancer cells to secrete senescence-associated secretory phenotype (SASP), which contributed to inhibition of tumor cell proliferation, and resulted in the suppression of HCC tumorigenesis. Together, our study provided mechanistic insights into a critical role of miat as a miRNA sponge in HCC cellular senescence, which might offer a potential therapeutic strategy for HCC treatment.

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p53-dependent growth arrest and induction of p21: A critical role for PCAF-mediated histone acetylation

Abstract: Comment on: Love IM, et al. Cell Cycle 2012; 11:2458-66

Cited by 20 publications

References 9 publications

RETRACTED: YY1 suppresses proliferation and migration of pancreatic ductal adenocarcinoma by regulating the CDKN3/MdM2/P53/P21 signaling pathway

RETRACTED: YY1 suppresses proliferation and migration of pancreatic ductal adenocarcinoma by regulating the CDKN3/MdM2/P53/P21 signaling pathway

Polysaccharide from angelica sinensis attenuates SNP-Induced Apoptosis in osteoarthritis Chondrocytes by Inducing Autophagy via ERK1/2 Pathway

lncRNA miat functions as a ceRNA to upregulate sirt1 by sponging miR-22-3p in HCC cellular senescence

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