scholarly journals Diallyl trisulfide-induced apoptosis in human cancer cells is linked to checkpoint kinase 1-mediated mitotic arrest

2009 ◽  
Vol 48 (11) ◽  
pp. 1018-1029 ◽  
Author(s):  
Dong Xiao ◽  
Yan Zeng ◽  
Shivendra V. Singh
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
Mitotic Arrest ◽  
Diallyl Trisulfide ◽  
Checkpoint Kinase ◽  
Checkpoint Kinase 1 ◽  
Human Cancer Cells ◽  
Induced Apoptosis

Characterization of novel Checkpoint kinase 1 inhibitors by in vitro assays and in human cancer cells treated with topoisomerase inhibitors

Life Sciences ◽  
2011 ◽  
Vol 89 (7-8) ◽  
pp. 259-268 ◽  
Author(s):  
Gilles Ferry ◽  
Aurélie Studeny ◽  
Céline Bossard ◽  
Philip M. Kubara ◽  
Denis Zeyer ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
In Vitro Assays ◽  
Topoisomerase Inhibitors ◽  
Checkpoint Kinase ◽  
Checkpoint Kinase 1 ◽  
Human Cancer Cells

p53 acetylation enhances Taxol-induced apoptosis in human cancer cells

APOPTOSIS ◽  
2012 ◽  
Vol 18 (1) ◽  
pp. 110-120 ◽  
Author(s):  
Jae Hyeong Kim ◽  
Eun-Kyung Yoon ◽  
Hye-Jin Chung ◽  
Seong-Yeol Park ◽  
Kyeong-Man Hong ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
Human Cancer Cells ◽  
Induced Apoptosis

scholarly journals RuvBL1 Maintains Resistance to TRAIL-Induced Apoptosis by Suppressing c-Jun/AP-1 Activity in Non-Small Cell Lung Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Hao Li ◽  
Taoran Zhou ◽  
Yue Zhang ◽  
Hengyi Jiang ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Therapeutic Strategy ◽  
Molecular Mechanisms ◽  
Human Cancer ◽  
Human Cancer Cells ◽  
The Common ◽  
Trail Resistance ◽  
Induced Apoptosis ◽  
Necrosis Factor

Lung cancer is the common malignant tumor with the highest death rate in the world. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) as a potential anticancer agent induces selective apoptotic death of human cancer cells. Unfortunately, approximately half of lung cancer cell lines are intrinsically resistant to TRAIL-induced cell death. In this study, we identified RuvBL1 as a repressor of c-Jun/AP-1 activity, contributing to TRAIL resistance in lung cancer cells. Knocking down RuvBL1 effectively sensitized resistant cells to TRAIL, and overexpression of RuvBL1 inhibited TRAIL-induced apoptosis. Moreover, there was a negative correlation expression between RuvBL1 and c-Jun in lung adenocarcinoma by Oncomine analyses. High expression of RuvBL1 inversely with low c-Jun in lung cancer was associated with a poor overall prognosis. Taken together, our studies broaden the molecular mechanisms of TRAIL resistance and suggest the application of silencing RuvBL1 synergized with TRAIL to be a novel therapeutic strategy in lung cancer treatment.

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