Staurosporine-induced G(1) arrest in cancer cells depends on an intact pRB but is independent of p16 status.

Abstract:

:Staurosporine and its derivative 7-hydroxystaurosporine are protein kinase inhibitors that are being considered for treatments of cancers. Several recent studies have shown that cells with defective pRB protein are resistant to the G(1) cell cycle-inhibiting effects of staurosporine compounds. In this study, we examined the effect of staurosporine on two breast cancer-derived and three lung cancer-derived cell lines characterized by deficiencies in the p16 tumor suppressor. All of these p16-deficient cell lines are highly sensitive to staurosporine-induced inhibition of pRB phosphorylation and induction of arrest in G(1). This response is similar to that seen in cultured normal human bronchial epithelial cells and normal mammary epithelial cells, but strikingly different than the staurosporine resistance seen in cancer cells with defective pRB. Interestingly, inhibition of pRB phosphorylation could be seen within 4 h of treatment, suggesting that this inhibition is a consequence of direct effects of staurosporine on protein kinase(s) rather than a result of induction of other cyclin-dependent kinase inhibitors. Our findings suggest that different types of cancer cells have vastly different responses to the staurosporine class of agents, and that evaluation of pRB and p16 will help predict the response of the cancer cells to these agents.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Zhou W,Lin Y,Wersto R,Chrest J,Gabrielson E

doi

10.1016/s0304-3835(02)00101-5

keywords:

subject

Has Abstract

pub_date

2002-09-08 00:00:00

pages

103-7

issue

1

eissn

0304-3835

issn

1872-7980

pii

S0304383502001015

journal_volume

183

pub_type

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