Triphenylstannyl((arylimino)methyl)benzoates with selective potency that induce G1 and G2/M cell cycle arrest and trigger apoptosis via ROS in human cervical cancer cells

2018 ◽  
Vol 47 (6) ◽  
pp. 1993-2008 ◽  
Author(s):  
Tushar S. Basu Baul ◽  
Imliwati Longkumer ◽  
Andrew Duthie ◽  
Priya Singh ◽  
Biplob Koch ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cancer Cells ◽  
M Cell ◽  
Cycle Arrest ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Excellent Selectivity ◽  
Human Cervical Cancer

Newly synthesized triphenylstannyl 4-((arylimino)methyl)benzoates show enhanced cytotoxicity and excellent selectivity in vitro towards human cervical cancer cells.

Notch1 induces cell cycle arrest and apoptosis in human cervical cancer cells: involvement of nuclear factor kappa B inhibition

2007 ◽  
Vol 17 (2) ◽  
pp. 502-510 ◽  
Author(s):  
J. Yao ◽  
L. Duan ◽  
M. Fan ◽  
J. Yuan ◽  
X. Wu
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Cycle Arrest ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

Notch signaling can serve as a tumor suppressor or tumor promoter in the same kind of cancer, such as human papillomavirus–positive cervical cancer cells. However, the exact mechanisms remain poorly characterized. Our studies demonstrated that constitutively overexpressed active Notch1 via stable transfection with exogenous intracellular domain of Notch1 (ICN) resulted in growth inhibition of the human cervical cancer cell line HeLa by inducing G2–M arrest and apoptosis. Moreover, the growth inhibition was correlated with inhibition of nuclear factor kappa B (NF-κB) p50 activation, accompanied by a decrease in the nuclear expression of NF-κB p50 and an increase in the cytosolic expression of IκBα. Consistent with these results, downregulation of cyclin D1 and Bcl-2, which are both the downstream genes of NF-κB, were observed in ICN-overexpressed cells. Overall, our results suggest that NF-κB inhibition may contribute partially to cell cycle arrest and apoptosis induced by Notch1 activation in human cervical cancer cells.

scholarly journals Caffeic acid phenethyl ester induces E2F-1-mediated growth inhibition and cell-cycle arrest in human cervical cancer cells

FEBS Journal ◽  
2013 ◽  
Vol 280 (11) ◽  
pp. 2581-2593 ◽  
Author(s):  
Tzu-Hui Hsu ◽  
Chin-Chen Chu ◽  
Mei-Whey Hung ◽  
Hwei-Jen Lee ◽  
Hsien-Jun Hsu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Caffeic Acid ◽  
Caffeic Acid Phenethyl Ester ◽  
Cycle Arrest ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

scholarly journals Recombinant Bacillus caldovelox Arginase Mutant (BCA-M) Induces Apoptosis, Autophagy, Cell Cycle Arrest and Growth Inhibition in Human Cervical Cancer Cells

2020 ◽  
Vol 21 (20) ◽  
pp. 7445 ◽  
Author(s):  
Sai-Fung Chung ◽  
Chi-Fai Kim ◽  
Ho-Yin Chow ◽  
Hiu-Chi Chong ◽  
Suet-Ying Tam ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Phase Iii ◽  
Protective Mechanism ◽  
Cycle Arrest ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

With our recent success in developing a recombinant human arginase drug against broad-spectrum cancer cell lines, we have explored the potential of a recombinant Bacillus caldovelox arginase mutant (BCA-M) for human cervical cancer treatment. Our studies demonstrated that BCA-M significantly inhibited the growth of human cervical cancer cells in vitro regardless of argininosuccinate synthetase (ASS) and argininosuccinate lyase (ASL) expression. Drug susceptibilities correlate well with the expressions of major urea cycle genes and completeness of L-arginine regeneration pathways. With the expressions of ASS and ASL genes conferring resistance to L-arginine deiminase (ADI) which is undergoing Phase III clinical trial, BCA-M offers the advantage of a broader spectrum of susceptible cancer cells. Mechanistic studies showed that BCA-M inhibited the growth of human cervical cancer cells by inducing apoptosis and cell cycle arrest at S and/or G2/M phases. Our results also displayed that autophagy served as a protective mechanism, while the growth inhibitory effects of BCA-M could be enhanced synergistically by its combination to the autophagy inhibitor, chloroquine (CQ), on human cervical cancer cells.

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