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Upregulation of p27 cyclin-dependent kinase inhibitor and a C-terminus truncated form of p27 contributes to G1 phase arrest
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Upregulation of p27 cyclin-dependent kinase inhibitor and a C-terminus truncated form of p27 contributes to G1 phase arrest
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Journal Article
Upregulation of p27 cyclin-dependent kinase inhibitor and a C-terminus truncated form of p27 contributes to G1 phase arrest
2016
Overview
Potent anti-cancer compounds FR901464 and its methyl-ketal derivative spliceostatin A (SSA) inhibit cell cycle progression at G1 and G2/M phases. These compounds bind to the spliceosome and inhibit the splicing reaction. However, the molecular mechanism underlying G1 arrest after SSA treatment remains unknown. In this study, we found that ~90% of SSA-treated cells arrested at G1 phase after cell cycle synchronization. SSA treatment caused upregulation of the p27 cyclin-dependent kinase inhibitor both at mRNA and protein levels. In addition to p27, we observed expression of p27*, a C-terminal truncated form of p27 that is translated from
CDKN1B
(p27) pre-mRNA accumulated after splicing inhibition. Overexpression of p27 or p27* inhibited the exit from G1 phase after a double thymidine block. Conversely, knocking down of p27 by siRNA partially suppressed the G1 phase arrest caused by SSA treatment. There results suggest that G1 arrest in SSA-treated cells is caused, at least in part, by upregulation of p27 and p27*.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/31
/ 38
/ 38/39
/ 38/90
/ 82
/ Antineoplastic Agents - toxicity
/ Cyclin-Dependent Kinase Inhibitor p27 - antagonists & inhibitors
/ Cyclin-Dependent Kinase Inhibitor p27 - genetics
/ Cyclin-Dependent Kinase Inhibitor p27 - metabolism
/ G1 Phase Cell Cycle Checkpoints - drug effects
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Proteins
/ RNA, Small Interfering - metabolism
/ Science
