Cell cycle arrest and apoptotic induction in LNCaP cells by MCS-C2, novel cyclin-dependent kinase inhibitor, through p53/p21(WAF1/CIP1) pathway
- Authors
- Park, Hae Young; Kim, Min Kyoung; Moon, Sang-Ik; Cho, Youl-Hee; Lee, Chul-Hoon
- Issue Date
- May-2006
- Publisher
- Oxford University Press
- Citation
- Cancer Science, v.97, no.5, pp 430 - 436
- Pages
- 7
- Indexed
- SCIE
SCOPUS
- Journal Title
- Cancer Science
- Volume
- 97
- Number
- 5
- Start Page
- 430
- End Page
- 436
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/44941
- DOI
- 10.1111/j.1349-7006.2006.00195.x
- ISSN
- 1347-9032
1349-7006
- Abstract
- The purpose of the present study was to investigate the mechanisms involved in the antiproliferative and apoptotic effects of MCS-C2, a novel analog of the pyrrolo[2,3-d]pyrimidine nucleoside toyocamycin and sangivamycin, in human prostate cancer LNCaP cells. MCS-C2, a selective inhibitor of cyclin-dependent kinase, was found to inhibit cell growth in a time- and dose-dependent manner, and inhibit cell cycle progression by inducing the arrest of the G1 phase and apoptosis in LNCaP cells. When treated with 3 mu M MCS-C2, inhibited proliferation associated with apoptotic induction was found in the LNCaP cells in a concentration and time-dependent manner, and nuclear DAPI staining revealed the typical nuclear features of apoptosis. Furthermore, MCS-C2 induced cell cycle arrest in the G1 phase through the upregulated phosphorylation of the p53 protein at Ser-15 and activation of its downstream target gene p21(WAF1/CIP1). Accordingly, these results suggest that MCS-C2 inhibits the proliferation of LNCaP cells by way of G1-phase arrest and apoptosis in association with the regulation of multiple molecules in the cell cycle progression.
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