scholarly journals Disruption of G1-phase phospholipid turnover by inhibition of Ca2+-independent phospholipase A2 induces a p53-dependent cell-cycle arrest in G1 phase

2006 ◽  
Vol 119 (6) ◽  
pp. 1005-1015 ◽  
Author(s):  
X. H. Zhang
Keyword(s):  
Cell Cycle ◽  
Phospholipase A2 ◽  
Cell Cycle Arrest ◽  
G1 Phase ◽  
Phospholipid Turnover ◽  
Cycle Arrest ◽  
Dependent Cell

scholarly journals Cannabidiol Induces Cell Cycle Arrest and Cell Apoptosis in Human Gastric Cancer SGC-7901 Cells

Biomolecules ◽  
2019 ◽  
Vol 9 (8) ◽  
pp. 302 ◽  
Author(s):  
Xin Zhang ◽  
Yao Qin ◽  
Zhaohai Pan ◽  
Minjing Li ◽  
Xiaona Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Protein Expression ◽  
Cell Cycle Arrest ◽  
Phase Cell ◽  
G1 Phase ◽  
Therapeutic Effects ◽  
Human Gastric Cancer ◽  
Expression Levels ◽  
Cycle Arrest

The main chemical component of cannabis, cannabidiol (CBD), has been shown to have antitumor properties. The present study examined the in vitro effects of CBD on human gastric cancer SGC-7901 cells. We found that CBD significantly inhibited the proliferation and colony formation of SGC-7901 cells. Further investigation showed that CBD significantly upregulated ataxia telangiectasia-mutated gene (ATM) and p53 protein expression and downregulated p21 protein expression in SGC-7901 cells, which subsequently inhibited the levels of CDK2 and cyclin E, thereby resulting in cell cycle arrest at the G0–G1 phase. In addition, CBD significantly increased Bax expression levels, decreased Bcl-2 expression levels and mitochondrial membrane potential, and then upregulated the levels of cleaved caspase-3 and cleaved caspase-9, thereby inducing apoptosis in SGC-7901 cells. Finally, we found that intracellular reactive oxygen species (ROS) increased after CBD treatment. These results indicated that CBD could induce G0–G1 phase cell cycle arrest and apoptosis by increasing ROS production, leading to the inhibition of SGC-7901 cell proliferation, thereby suggesting that CBD may have therapeutic effects on gastric cancer.

Inhibition of cell growth and induction of G1-phase cell cycle arrest in hepatoma cells by steroid extract from Meretrix meretrix

2006 ◽  
Vol 232 (2) ◽  
pp. 199-205 ◽  
Author(s):  
Ting-He Wu ◽  
Ruo-Lin Yang ◽  
Li-Ping Xie ◽  
Hong-Zhong Wang ◽  
Lei Chen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Cell Cycle Arrest ◽  
Hepatoma Cells ◽  
Phase Cell ◽  
G1 Phase ◽  
Meretrix Meretrix ◽  
Cycle Arrest

scholarly journals MdmX Protects p53 from Mdm2-Mediated Degradation

2000 ◽  
Vol 20 (3) ◽  
pp. 1001-1007 ◽  
Author(s):  
Mark W. Jackson ◽  
Steven J. Berberich
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Nuclear Export ◽  
P53 Protein ◽  
Ring Finger ◽  
Ring Finger Domain ◽  
Cycle Arrest ◽  
Dependent Cell ◽  
Potential Basis ◽  
P53 Tumor Suppressor Protein

ABSTRACT The p53 tumor suppressor protein is stabilized in response to cellular stress, resulting in activation of genes responsible for either cell cycle arrest or apoptosis. The cellular pathway for releasing normal cells from p53-dependent cell cycle arrest involves the Mdm2 protein. Recently, a p53-binding protein with homology to Mdm2 was identified and called MdmX. Like Mdm2, MdmX is able to bind p53 and inhibit p53 transactivation; however, the ability of MdmX to degrade p53 has yet to be examined. We report here that MdmX is capable of associating with p53 yet is unable to facilitate nuclear export or induce p53 degradation. In addition, expression of MdmX can reverse Mdm2-targeted degradation of p53 while maintaining suppression of p53 transactivation. Using a series of MdmX deletions, we have determined that there are two distinct domains of the MdmX protein that can stabilize p53 in the presence of Mdm2. One domain requires MdmX interaction with p53 and results in the retention of both proteins within the nucleus and repression of p53 transactivation. The second domain involves the MdmX ring finger and results in stabilization of p53 and an increase in p53 transactivation. The potential basis for stabilization and increased p53 transactivation by the MdmX ring finger domain is discussed. Based on these observations, we propose that the MdmX protein may function to maintain a nuclear pool of p53 protein in undamaged cells.

scholarly journals Enforced Expression of p14ARF Induces p53-Dependent Cell Cycle Arrest but Not Apoptosis

Cell Cycle ◽  
2005 ◽  
Vol 4 (3) ◽  
pp. 465-472 ◽  
Author(s):  
Stuart Gallagher ◽  
Richard F. Kefford ◽  
Helen Rizos
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Dependent Cell

Hypoxia Induces Resistance to 5-Fluorouracil in Oral Cancer Cells Via G1 Phase Cell Cycle Arrest

2009 ◽  
pp. 184-190
Author(s):  
Sayaka Yoshiba ◽  
Daisuke Ito ◽  
Tatsuhito Nagumo ◽  
Tatsuo Shirota ◽  
Masashi Hatori ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Oral Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Phase Cell ◽  
G1 Phase ◽  
Cycle Arrest ◽  
Oral Cancer Cells
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