@article {OHNO699, author = {YOSHIFUMI OHNO and RUIRONG YI and AKIKO SUGANAMI and YUTAKA TAMURA and AKIO MATSUMOTO and SHOJI MATSUMOTO and KENGO SAITO and HIROSHI SHIRASAWA}, title = {CCL299, a Benzimidazole Derivative Induces G1 Phase Arrest and Apoptosis in Cancer Cells}, volume = {41}, number = {2}, pages = {699--706}, year = {2021}, doi = {10.21873/anticanres.14821}, publisher = {International Institute of Anticancer Research}, abstract = {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 non-cancer cells and TIG-1-20 fibroblasts. Flow cytometry, western blotting, and caspase-3/7 assays revealed that CCL299 induced G1-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 p-CDK2 (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.}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/41/2/699}, eprint = {https://ar.iiarjournals.org/content/41/2/699.full.pdf}, journal = {Anticancer Research} }