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Decreased skp2 expression is necessary but not sufficient for therapy-induced senescence in prostate cancer.

Abstract：

:Therapy-induced senescence (TIS), a cytostatic stress response in cancer cells, is induced inefficiently by current anticancer agents and radiation. The mechanisms that mediate TIS in cancer cells are not well defined. Herein, we characterize a robust senescence response both in vitro and in vivo to the quinone diaziquone (AZQ), previously identified in a high-throughput senescence-induction small-molecule screen. Using AZQ and several other agents that induce senescence, we screened a series of cyclin-dependent kinase inhibitors and found that p27(Kip1) was induced in all investigated prostate cancer cell lines. The ubiquitin-ligase Skp2 negatively regulates p27(Kip1) and, during TIS, is translocated to the cytoplasm before its expression is decreased in senescent cells. Overexpression of Skp2 blocks the effects of AZQ on senescence and p27(Kip1) induction. We also find that stable long-term short hairpin RNA knockdown of Skp2 decreases proliferation but does not generate the complete senescence phenotype. We conclude that Skp2 participates in regulating TIS but, alone, is insufficient to induce senescence in cancer cells.

journal_name

Transl Oncol

journal_title

Translational oncology

authors

Ewald JA,Jarrard DF

doi

10.1593/tlo.12181

subject

Has Abstract

pub_date

2012-08-01 00:00:00

pages

278-87

issue

4

issn

1936-5233

journal_volume

5

pub_type

杂志文章

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