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The human cyclin B1 protein modulates sensitivity of DNA mismatch repair deficient prostate cancer cell lines to alkylating agents.

Abstract：

:DNA damage caused by alkylating agents results in a G2 checkpoint arrest. DNA mismatch repair (MMR) deficient cells are resistant to killing by alkylating agents and are unable to arrest the cell cycle in G2 phase after alkylation damage. We investigated the response of two MMR-deficient prostate cancer cell lines DU145 and LNCaP to the alkylating agent MNNG. Our studies reveal that DU145 cancer cells are more sensitive to killing by MNNG than LNCaP. Investigation of the underlying reasons for lower resistance revealed that the DU145 cells contain low endogenous levels of cyclin B1. We provide direct evidence that the endogenous level of cyclin B1 modulates the sensitivity of MMR-deficient prostate cancer cells to alkylating agents.

journal_name

Exp Cell Res

journal_title

Experimental cell research

authors

Rasmussen LJ,Rasmussen M,Lützen A,Bisgaard HC,Singh KK

doi

10.1006/excr.2000.4865

keywords:

subject

Has Abstract

pub_date

2000-05-25 00:00:00

pages

127-34

issue

1

eissn

0014-4827

issn

1090-2422

pii

S0014-4827(00)94865-1

journal_volume

257

pub_type

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