Journal
ANTICANCER RESEARCH
Volume 41, Issue 2, Pages 699-706Publisher
INT INST ANTICANCER RESEARCH
DOI: 10.21873/anticanres.14821
Keywords
Benzimidazole; apoptosis; G(1) phase arrest; CDK2; p21; p53
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CCL299 exhibits cytotoxic activity via apoptosis in a subset of cancer cells, while showing no significant cytotoxic effects on noncancer cells.
Background/Aim: Benzimidazoles are considered potential anticancer candidates. We herein studied the anticancer activity of CCL299, 4-(1H-1,3-benzodiazol-1-yl) benzonitrile. Materials and Methods: In this in vitro study, we used ATP assays, flow cytometry, western blotting, and caspase-3/7 assays to evaluate the effects of CCL299 on cell proliferation, cell-cycle progression and apoptosis. Results: ATP assays showed that CCL299 inhibited cell growth in the hepatoblastoma cell line HepG2 and the cervical cancer cell line HEp-2, without exhibiting cytotoxic effects on noncancer cells and TIG-1-20 fibroblasts. Flow cytometry, western blotting, and caspase-3/7 assays revealed that CCL299 induced G(1)-phase cell-cycle arrest followed by apoptosis that was associated with up-regulation of p-p53 (Ser15) and p21 expression and the down-regulation of pCDK2 (Thr160) expression. Conclusion: CCL299 exhibits cytotoxic activity via apoptosis in a subset of cancer cells, and should be considered as a promising anticancer candidate agent.
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