scholarly journals Tumor suppressor BLU inhibits proliferation of nasopharyngeal carcinoma cells by regulation of cell cycle, c-Jun N-terminal kinase and the cyclin D1 promoter

BMC Cancer ◽  
2012 ◽  
Vol 12 (1) ◽  
Author(s):  
Xiangning Zhang ◽  
Hui Liu ◽  
Binbin Li ◽  
Peichun Huang ◽  
Jianyong Shao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Nasopharyngeal Carcinoma ◽  
Tumor Suppressor ◽  
Cyclin D1 ◽  
Carcinoma Cells ◽  
Regulation Of Cell Cycle

Vitamin C affects G0/G1 cell cycle and autophagy by downregulating of cyclin D1 in gastric carcinoma cells

2021 ◽  
Vol 85 (3) ◽  
pp. 553-561
Author(s):  
Chenxia Ren ◽  
Cuiling Wu ◽  
Changqing Yang ◽  
Changhong Lian
Keyword(s):  
Cell Cycle ◽  
Gastric Carcinoma ◽  
Vitamin C ◽  
Cyclin D1 ◽  
Bioinformatics Analysis ◽  
Carcinoma Cells ◽  
Cell Cycle Pathway ◽  
Differential Gene ◽  
Regulation Of Cell Cycle ◽  
Amp Activated Protein Kinase

ABSTRACT Vitamin C has re-emerged as a promising anticancer agent. This study attempts to analyze the differential gene expression of profiles GSE11919 to look for some clues, and the most significant cell cycle pathway caused by vitamin C was identified by integrated bioinformatics analysis. Inspired by this, we investigated the effect of vitamin C treatment on gastric carcinoma cells by detection of cell cycle, apoptosis, and autophagy. Vitamin C significantly elevated the percentage of cells at G0/G1 phase, whereas the percentage of S phase cells was decreased. Meanwhile, vitamin C treatment resulted in downregulation of cell cycle-related protein Cyclin D1. We deduced that the downregulation of Cyclin D1 by vitamin C accompanied by significantly increased 5′AMP-activated protein kinase and induced autophagy in MKN45 cells. These results suggest that vitamin C has the antiproliferation effect on gastric carcinoma cells via the regulation of cell cycle and autophagy by Cyclin D1.

scholarly journals Alterations of cell cycle control proteins SHP-1/2, p16, CDK4 and cyclin D1 in radioresistant nasopharyngeal carcinoma cells

2014 ◽  
Vol 10 (4) ◽  
pp. 1709-1716 ◽  
Author(s):  
GANG PENG ◽  
RU-BO CAO ◽  
YUE-HUA LI ◽  
ZHEN-WEI ZOU ◽  
JING HUANG ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Nasopharyngeal Carcinoma ◽  
Cyclin D1 ◽  
Cell Cycle Control ◽  
Carcinoma Cells

scholarly journals Temporally distinct roles for tumor suppressor pathways in cell cycle arrest and cellular senescence in Cyclin D1-driven tumor

2012 ◽  
Vol 11 (1) ◽  
pp. 28 ◽  
Author(s):  
Hasan Zalzali ◽  
Mohamad Harajly ◽  
Lina Abdul-Latif ◽  
Nader El-Chaar ◽  
Ghassan Dbaibo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Cyclin D1 ◽  
Cell Cycle Arrest ◽  
Cellular Senescence ◽  
Cycle Arrest

scholarly journals Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid induces apoptosis and cell cycle arrest in CNE-2Z nasopharyngeal carcinoma cells

2013 ◽  
Vol 29 (6) ◽  
pp. 2101-2108 ◽  
Author(s):  
KEFENG WU ◽  
YI LIU ◽  
YINGNIAN LV ◽  
LIAO CUI ◽  
WENDE LI ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Nasopharyngeal Carcinoma ◽  
Cell Cycle Arrest ◽  
Carcinoma Cells ◽  
Cycle Arrest

scholarly journals The RASSF1A Tumor Suppressor Restrains Anaphase-Promoting Complex/Cyclosome Activity during the G1/S Phase Transition To Promote Cell Cycle Progression in Human Epithelial Cells

2008 ◽  
Vol 28 (10) ◽  
pp. 3190-3197 ◽  
Author(s):  
Angelique W. Whitehurst ◽  
Rosalyn Ram ◽  
Latha Shivakumar ◽  
Boning Gao ◽  
John D. Minna ◽  
...  
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Tumor Suppressor ◽  
Epithelial Cells ◽  
Cyclin D1 ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Phase Cell ◽  
Anaphase Promoting Complex ◽  
Cycle Progression

ABSTRACT Multiple molecular lesions in human cancers directly collaborate to deregulate proliferation and suppress apoptosis to promote tumorigenesis. The candidate tumor suppressor RASSF1A is commonly inactivated in a broad spectrum of human tumors and has been implicated as a pivotal gatekeeper of cell cycle progression. However, a mechanistic account of the role of RASSF1A gene inactivation in tumor initiation is lacking. Here we have employed loss-of-function analysis in human epithelial cells for a detailed investigation of the contribution of RASSF1 to cell cycle progression. We found that RASSF1A has dual opposing regulatory connections to G1/S phase cell cycle transit. RASSF1A associates with the Ewing sarcoma breakpoint protein, EWS, to limit accumulation of cyclin D1 and restrict exit from G1. Surprisingly, we found that RASSF1A is also required to restrict SCFβTrCP activity to allow G/S phase transition. This restriction is required for accumulation of the anaphase-promoting complex/cyclosome (APC/C) inhibitor Emi1 and the concomitant block of APC/C-dependent cyclin A turnover. The consequence of this relationship is inhibition of cell cycle progression in normal epithelial cells upon RASSF1A depletion despite elevated cyclin D1 concentrations. Progression to tumorigenicity upon RASSF1A gene inactivation should therefore require collaborating genetic aberrations that bypass the consequences of impaired APC/C regulation at the G1/S phase cell cycle transition.

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