C3. Mechanisms of human colon cancer cells sensitization to nitric oxide-induced apoptosis

Nitric Oxide ◽  
2007 ◽  
Vol 17 ◽  
pp. 20
Author(s):  
M. Cortier ◽  
J.F. Jeannin ◽  
A. Bettaieb
Keyword(s):  
Nitric Oxide ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Induced Apoptosis ◽  
Human Colon Cancer Cells

scholarly journals Transcriptome analysis reveals GA induced apoptosis in HCT116 human colon cancer cells through calcium and p53 signal pathways

RSC Advances ◽  
2018 ◽  
Vol 8 (22) ◽  
pp. 12449-12458 ◽  
Author(s):  
Chen Yang ◽  
Xiaoyu Xie ◽  
Hu Tang ◽  
Xuyan Dong ◽  
Xiaodong Zhang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Gallic Acid ◽  
Transcriptome Analysis ◽  
Human Colon ◽  
Signal Pathways ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Induced Apoptosis ◽  
Human Colon Cancer Cells

Gallic acid (GA) is a polyphenol widely found in plants that induced apoptosis in human colon cancer cells through calcium and p53 signal pathways.

Influence of the nitric oxide donor glyceryl trinitrate on apoptotic pathways in human colon cancer cells

2002 ◽  
Vol 123 (1) ◽  
pp. 235-246 ◽  
Author(s):  
Anne Millet ◽  
Ali Bettaieb ◽  
Flore Renaud ◽  
Laurent Prevotat ◽  
Arlette Hammann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Colon Cancer ◽  
Glyceryl Trinitrate ◽  
Cancer Cells ◽  
Human Colon ◽  
Nitric Oxide Donor ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Apoptotic Pathways ◽  
Human Colon Cancer Cells

scholarly journals SRL lectin induced apoptosis of human colon cancer cells: identification of pathways leading to cell death (589.1)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Nilanjan Guha ◽  
Deepak SA ◽  
Srikanth Barkeer ◽  
Arun KS ◽  
Jonathan Rhodes ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Induced Apoptosis ◽  
Human Colon Cancer Cells

scholarly journals Activation of PERK Contributes to Apoptosis and G2/M Arrest by Microtubule Disruptors in Human Colorectal Carcinoma Cells

Cancers ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 97 ◽  
Author(s):  
Ming-Shun Wu ◽  
Chih-Chiang Chien ◽  
Ganbolor Jargalsaikhan ◽  
Noor Andryan Ilsan ◽  
Yen-Chou Chen
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
B Cell Lymphoma ◽  
Human Colon ◽  
Cyclin B1 ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Jnk Inhibitors ◽  
Induced Apoptosis ◽  
Human Colon Cancer Cells

Microtubule-targeting agents (MTAs) are widely used in cancer chemotherapy, but the therapeutic responses significantly vary among different tumor types. Protein kinase RNA-like endoplasmic reticular (ER) kinase (PERK) is an ER stress kinase, and the role of PERK in the anticancer effects of MTAs is still undefined. In the present study, taxol (TAX) and nocodazole (NOC) significantly induced apoptosis with increased expression of phosphorylated PERK (pPERK; Tyr980) in four human colon cancer cell lines, including HCT-15, COLO205, HT-20, and LOVO cells. Induction of G2/M arrest by TAX and NOC with increases in phosphorylated Cdc25C and cyclin B1 protein were observed in human colon cancer cells. Application of the c-Jun N-terminal kinase (JNK) inhibitors SP600125 (SP) and JNK inhibitor V (JNKI) significantly reduced TAX- and NOC-induced apoptosis and G2/M arrest of human colon cancer cells. Interestingly, TAX- and NOC-induced pPERK (Tyr980) protein expression was inhibited by adding the JNK inhibitors, SP and JNKI, and application of the PERK inhibitor GSK2606414 (GSK) significantly reduced apoptosis and G2/M arrest by TAX and NOC, with decreased pPERK (Tyr980) and pJNK, phosphorylated Cdc25C, and Cyc B1 protein expressions in human colon cancer cells. Decreased viability by TAX and NOC was inhibited by knockdown of PERK using PERK siRNA in COLO205 and HCT-15 cells. Disruption of the mitochondrial membrane potential and an increase in B-cell lymphoma-2 (Bcl-2) protein phosphorylation (pBcl-2; Ser70) by TAX and NOC were prevented by adding the PERK inhibitor GSK and JNK inhibitor SP and JNKI. A cross-activation of JNK and PERK by TAX and NOC leading to anti-CRC actions including apoptosis and G2/M arrest was first demonstrated herein.

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