Reference - Detail
| RRC ID | 71643 |
|---|---|
| Author | Ohno Y, Yi R, Suganami A, Tamura Y, Matsumoto A, Matsumoto S, Saito K, Shirasawa H. |
| Title | CCL299, a Benzimidazole Derivative Induces G1 Phase Arrest and Apoptosis in Cancer Cells. |
| Journal | Anticancer Res |
| 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. |
| Volume | 41(2) |
| Pages | 699-706 |
| Published | 2021-2-1 |
| DOI | 10.21873/anticanres.14821 |
| PII | 41/2/699 |
| PMID | 33517274 |
| MeSH | A549 Cells Antineoplastic Agents / pharmacology* Apoptosis / drug effects* Benzimidazoles / pharmacology* Caspase 3 / metabolism Caspase 7 / metabolism Cyclin-Dependent Kinase 2 / metabolism Cyclin-Dependent Kinase Inhibitor p21 / metabolism Female G1 Phase Cell Cycle Checkpoints / drug effects* HeLa Cells Hep G2 Cells Humans Neoplasms / drug therapy* Neoplasms / metabolism Neoplasms / pathology Signal Transduction Tumor Suppressor Protein p53 / metabolism |
| IF | 1.994 |
| Resource | |
| Human and Animal Cells | HEp-2(RCB1889) |