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Suppression of mammary carcinoma growth in vitro and in vivo by inducible expression of the Cdk inhibitor p21.

Abstract：

:Mammary carcinomas that develop in C3 (1)/SV40 T- antigen (TAg) transgenic mice have lost the p53-mediated induction of p21, leading to increased cellular proliferation and significant elevations of cyclins and Cdks. To test whether p21 could serve as a target for anticancer therapy for this mammary cancer model, a retroviral delivery system for the inducible expression of p21 was developed. We demonstrate that overexpression of p21 in C3(1)/TAg mammary tumor cells using the retroviral inducible p21 expression system results in increased apoptosis, reduced cell proliferation in vitro and reduced tumor growth in vivo associated with reduced expression of cyclins D1 and E, and Cdks 2, 4, and 6. Reciprocal changes in the expression of p21 and p27(Kip1), another cell-cycle regulator, were also observed. Because reduced p21 expression occurs frequently in human breast cancer, restoration of the Cdk inhibitor p21 by gene therapy approaches may provide a method for inhibiting mammary tumor progression.

journal_name

Cancer Gene Ther

journal_title

Cancer gene therapy

authors

Shibata MA,Yoshidome K,Shibata E,Jorcyk CL,Green JE

doi

10.1038/sj.cgt.7700275

subject

Has Abstract

pub_date

2001-01-01 00:00:00

pages

23-35

issue

1

eissn

0929-1903

issn

1476-5500

journal_volume

8

pub_type

杂志文章

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