RRC ID 71643
著者 Ohno Y, Yi R, Suganami A, Tamura Y, Matsumoto A, Matsumoto S, Saito K, Shirasawa H.
タイトル CCL299, a Benzimidazole Derivative Induces G1 Phase Arrest and Apoptosis in Cancer Cells.
ジャーナル 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.
巻・号 41(2)
ページ 699-706
公開日 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
リソース情報
ヒト・動物細胞 HEp-2(RCB1889)