Induction of cell cycle arrest via the p21, p27–cyclin E,A/Cdk2 pathway in SMMC-7721 hepatoma cells by clioquinol

Huang, Zhiwei; Wang, Lianqiu; Chen, Lifeng; Zhang, Yifei; Shi, Ping

doi:10.1515/acph-2015-0034

Cited by 19 publications

(15 citation statements)

References 22 publications

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“…In addition, p53 can up-regulate p21 expression, which also promotes cell cycle arrest in the S phase [ 61 ]. Here, NaF increased p21 protein levels and mRNA expression (Figure 17 ), which is consistent with studies demonstrating that various stimuli induce cell cycle arrest in the S phase through p53-dependent activation of p21 [ 45 , 62 – 64 ]. P21 generally induces S-phase cell cycle arrest by inhibiting CDK2 activity [ 64 – 66 ] which, together with cyclin A, is necessary for the progression of cells through the S phase [ 67 ]; inactivation of cyclin A/CDK2 complexes prevents progression beyond the S phase checkpoint.…”

Section: Discussionsupporting

confidence: 90%

Sodium fluoride causes hepatocellular S-phase arrest by activating ATM-p53-p21 and ATR-Chk1-Cdc25A pathways in mice

et al. 2017

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In this study, experimental pathology, flow cytometry (FCM), quantitative real-time polymerase chain reaction (qRT-PCR), and western blot (WB) were used to evaluate the effects of sodium fluoride (NaF) on hepatocellular cell cycle progression in mice. A total of 240 ICR mice were divided equally into four groups; the experimental groups received 12, 24, or 48 mg/kg NaF intragastrically for 42 days, while the control group received distilled water. Doses of NaF above 12 mg/kg increased the percentage of cells in S phase (S-phase arrest), reduced percentages of cells in G0/G1 or G2/M phase, and activated the ATM-p53-p21 and ATR-Chk1-Cdc25A pathways. Activation of these pathways was characterized by up-regulation of ATM, p53, p21, ATR, and Chk1 mRNA and protein expression, and down-regulation of Cdc25A, cyclin E, cyclin A, CDK2, CDK4, and proliferating cell nuclear antigen (PCNA) mRNA and protein expression. These results indicate that NaF caused S-phase arrest by activating the ATM-p53-p21 and ATR-Chk1-Cdc25A pathways.

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Section: Discussionsupporting

confidence: 90%

Sodium fluoride causes hepatocellular S-phase arrest by activating ATM-p53-p21 and ATR-Chk1-Cdc25A pathways in mice

et al. 2017

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“…In addition, resveratrol inhibited cell proliferation of PASMCs induced by hypoxia in a dose-dependent manner. Protein expression levels of p21 and p27, which are established cyclin-dependent kinase inhibitors ( 27 , 28 ), were rescued from hypoxia following treatment with resveratrol, suggesting the potential role of resveratrol in regulating cell cycles. MMPs serve important roles in proliferation and metastasis of smooth muscle cells, and provide space for PASMCs to migrate and proliferate around surrounding tissues.…”

Section: Discussionmentioning

confidence: 97%

Resveratrol inhibits hypoxia-induced proliferation and migration of pulmonary artery vascular smooth muscle cells by inhibiting the phosphoinositide 3-kinase/protein kinase B signaling pathway

Guan

Шен

Liang

et al. 2017

Molecular Medicine Reports

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Hypoxia is a risk factor for severe chronic obstructive pulmonary disease, which aggravates the disease and may cause mortality by inducing hypoxic pulmonary hypertension (HPH). Proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) may mediate this effect. Resveratrol is a phenolic compound extracted from a plant and has been reported to alleviate HPH, although the underlying mechanisms remained to be elucidated. In cancer, resveratrol has been reported to abrogate the phosphoinositide 3-kinase/protein kinase B (AKT) signaling pathway, thereby inhibiting tumor development. Therefore, the present study aimed to investigate the role of resveratrol in preventing PASMCs from proliferating and migrating. Resveratrol was demonstrated to be inhibitory in a dose-dependent manner on hypoxia-induced cell proliferation and migration, and protein expression levels of phosphorylated AKT and AKT. Additionally, resveratrol was identified to act synergistically with LY-294002, a phosphorylation inhibitor of AKT, but antagonistically with insulin-like growth factor-1, an agonist of AKT phosphorylation. This suggested that resveratrol may reduce proliferation and migration by diminishing expression and phosphorylation of AKT, thereby preventing development of HPH.

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“…Cyclin D1 and cyclin E are important members of cyclin family, which are upregulated in human lung cancer cells and regulates the progression of the cell cycle by controlling G1/S transition [ 17 – 20 ]. p27 is frequently downregulated in tumor cells, which functions as a CDK inhibitor and causes cell cycle arrest in the G1 phase [ 21 – 24 ]. These results was in accordance with the fact that TRIM22 could facilitate cell cycle transition, indicating a oncogenic function of TRIM22 in lung cancer cells.…”

Section: Discussionmentioning

confidence: 99%

TRIM22 confers poor prognosis and promotes epithelial-mesenchymal transition through regulation of AKT/GSK3β/β-catenin signaling in non-small cell lung cancer

et al. 2017

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Expression pattern and biological roles of TRIM22 remains unknown in most human cancers. The present study aims to discover its clinical significance and function in human non-small cell lung cancer (NSCLC). Immunohistochemistry was used to examine TRIM22 expression in 126 cases of NSCLC specimens. TRIM22 protein was upregulated in 70/126 (55.6%) non-small cell lung cancer tissues compared with normal lung tissue. TRIM22 overexpression was associated with advanced TNM stage, positive nodal metastasis and poor prognosis. Plasmid and siRNA transfection were performed in lung cancer cell lines. TRIM22 overexpression promoted proliferation, colony formation and invasion in A549 cells. While its depletion exhibited the opposite effects in H1299 cell line. TRIM22 overexpression promoted cell cycle progression through regulation of cyclin D1, cyclin E and p27. TRIM22 also changed the expression of epithelial to mesenchymal transition (EMT) markers including E-cadherin N-cadherin, Vimentin and Snail. Furthermore, TRIM22 activated PI3K/AKT/GSK3β/β-catenin oncogenic signaling pathways. Treatment with PI3K inhibitor LY294002 and β-catenin siRNA blocked the effects of TRIM22 on EMT in TRIM22-overexpressing cells. In conclusion,TRIM22 serves as an important oncoprotein and a promoter of cell proliferation and invasion through AKT/ GSK3β/β-catenin induced EMT in NSCLC.

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Induction of cell cycle arrest via the p21, p27–cyclin E,A/Cdk2 pathway in SMMC-7721 hepatoma cells by clioquinol

Cited by 19 publications

References 22 publications

Sodium fluoride causes hepatocellular S-phase arrest by activating ATM-p53-p21 and ATR-Chk1-Cdc25A pathways in mice

Sodium fluoride causes hepatocellular S-phase arrest by activating ATM-p53-p21 and ATR-Chk1-Cdc25A pathways in mice

Resveratrol inhibits hypoxia-induced proliferation and migration of pulmonary artery vascular smooth muscle cells by inhibiting the phosphoinositide 3-kinase/protein kinase B signaling pathway

TRIM22 confers poor prognosis and promotes epithelial-mesenchymal transition through regulation of AKT/GSK3β/β-catenin signaling in non-small cell lung cancer

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