scholarly journals Wound Healing Activity of a Novel Formulation SKRIN via Induction of Cell Cycle Progression and Inhibition of PCNA–p21 Complex Interaction Leading to Cell Survival and Proliferation

2021 ◽  
Author(s):  
Swatantra Kumar ◽  
Vimal K. Maurya ◽  
Sai V. Chitti ◽  
Russell Kabir ◽  
Karuna Shanker ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Wound Healing ◽  
Cell Survival ◽  
Cell Cycle Progression ◽  
Complex Interaction ◽  
Cycle Progression ◽  
Wound Healing Activity ◽  
Cell Survival And Proliferation

A novel CyclinE/CyclinA-CDK Inhibitor targets p27Kip1 degradation, cell cycle progression and cell survival: Implications in cancer therapy

2013 ◽  
Vol 333 (1) ◽  
pp. 103-112 ◽  
Author(s):  
Lu Dai ◽  
Yuqing Liu ◽  
Junyang Liu ◽  
Xiaoming Wen ◽  
ZhengShuang Xu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cancer Therapy ◽  
Cell Survival ◽  
Cell Cycle Progression ◽  
Cdk Inhibitor ◽  
Cycle Progression

scholarly journals gp130-Mediated Stat3 Activation in Enterocytes Regulates Cell Survival and Cell-Cycle Progression during Colitis-Associated Tumorigenesis

Cancer Cell ◽  
2009 ◽  
Vol 15 (2) ◽  
pp. 91-102 ◽  
Author(s):  
Julia Bollrath ◽  
Toby J. Phesse ◽  
Vivian A. von Burstin ◽  
Tracy Putoczki ◽  
Moritz Bennecke ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Survival ◽  
Cell Cycle Progression ◽  
Cycle Progression

scholarly journals Enrichment of the  -catenin-TCF complex at the S and G2 phases ensures cell survival and cell cycle progression

2014 ◽  
Vol 127 (22) ◽  
pp. 4833-4845 ◽  
Author(s):  
Y. Ding ◽  
S. Su ◽  
W. Tang ◽  
X. Zhang ◽  
S. Chen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Survival ◽  
Cell Cycle Progression ◽  
Cycle Progression

ESM-1 silencing decreased cell survival, migration, and invasion and modulated cell cycle progression in hepatocellular carcinoma

Amino Acids ◽  
2010 ◽  
Vol 40 (3) ◽  
pp. 1003-1013 ◽  
Author(s):  
Yun Hee Kang ◽  
Na Young Ji ◽  
Chung Il Lee ◽  
Hee Gu Lee ◽  
Jae Wha Kim ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Survival ◽  
Cell Cycle Progression ◽  
Migration And Invasion ◽  
Cycle Progression

scholarly journals Interference with 3′,5′-Cyclic Adenosine Monophosphate Response Element Binding Protein Stimulates Apoptosis through Aberrant Cell Cycle Progression and Checkpoint Activation

2006 ◽  
Vol 20 (5) ◽  
pp. 1112-1120 ◽  
Author(s):  
Jessica H. Dworet ◽  
Judy L. Meinkoth
Keyword(s):  
Cell Cycle ◽  
Protein Kinase ◽  
Cell Survival ◽  
Protein Kinase A ◽  
Cell Cycle Progression ◽  
Thyroid Cell ◽  
Checkpoint Activation ◽  
Cycle Progression ◽  
Element Binding Protein ◽  
Kinase A

Abstract We previously reported that protein kinase A activity is an important determinant of thyroid cell survival. Given the important role of cAMP response element binding protein (CREB) in mediating the transcriptional effects of protein kinase A, we explored whether interference with CREB family members impaired thyroid cell survival. Expression of A-CREB, a dominant-negative CREB mutant that inhibits CREB DNA binding activity, induced apoptosis in rat thyroid cells. A-CREB inhibited CRE-regulated gene expression but failed to alter the expression of bcl-2 family members or of well-characterized inhibitors of apoptosis. To elucidate the mechanism through which impaired CREB function triggered apoptosis, its effects on cell proliferation were examined. Expression of A-CREB inhibited cell number increases, in part due to delayed cell cycle transit. Protracted S-phase progression in A-CREB-expressing cells was sufficient to activate a checkpoint response characterized by Chk-1, histone H2A.X, and p53 phosphorylation. To determine whether cell cycle progression was required for apoptosis, the effects of p27 overexpression were investigated. Overexpression of p27 prevented cell cycle progression, checkpoint activation, and apoptosis in A-CREB-expressing cells. These data reveal a novel mechanism through which interference with CREB abrogates cell survival, through checkpoint activation secondary to cell cycle delay. This study may explain how interference with CREB induces apoptosis in cells where alterations in the expression of pro- and anti-survival genes are not detected.

scholarly journals The p57 CDKi integrates stress signals into cell-cycle progression to promote cell survival upon stress

2012 ◽  
Vol 31 (13) ◽  
pp. 2952-2964 ◽  
Author(s):  
Manel Joaquin ◽  
Albert Gubern ◽  
Daniel González-Nuñez ◽  
E Josué Ruiz ◽  
Isabel Ferreiro ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Survival ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Promote Cell Survival ◽  
Stress Signals

scholarly journals Distinct Signaling Pathways Mediate Stimulation of Cell Cycle Progression and Prevention of Apoptotic Cell Death by Estrogen in Rat Pituitary Tumor PR1 Cells

2003 ◽  
Vol 14 (12) ◽  
pp. 5051-5059 ◽  
Author(s):  
Simona Caporali ◽  
Manami Imai ◽  
Lucia Altucci ◽  
Massimo Cancemi ◽  
Silvana Caristi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Death ◽  
Dna Synthesis ◽  
Cell Survival ◽  
Pituitary Tumor ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Rat Pituitary ◽  
Stimulation Of

Estrogens control cell growth and viability in target cells via an interplay of genomic and extragenomic pathways not yet elucidated. Here, we show evidence that cell proliferation and survival are differentially regulated by estrogen in rat pituitary tumor PR1 cells. Pico- to femtomolar concentrations of 17β-estradiol (E2) are sufficient to foster PR1 cell proliferation, whereas nanomolar concentrations of the same are needed to prevent cell death that occurs at a high rate in these cells in the absence of hormone. Activation of endogenous (PRL) or transfected estrogen-responsive genes occurs at the same, higher concentrations of E2 required to promote cell survival, whereas stimulation of cyclin D3 expression and DNA synthesis occur at lower E2 concentrations. Similarly, the pure antiestrogen ICI 182,780 inhibits estrogen response element-dependent trans-activation and cell death more effectively than cyclin-cdk activity, G1-S transition, or DNA synthesis rate. In antiestrogen-treated and/or estrogen-deprived cells, death is due predominantly to apoptosis. Estrogen-induced cell survival, but not E2-dependent cell cycle progression, can be prevented by an inhibitor of c-Src kinase or by blockade of the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling pathway. These data indicate the coexistence of two distinguishable estrogen signaling pathways in PR1 cells, characterized by different functions and sensitivity to hormones and antihormones.

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