EARLY GENE RESPONSES ASSOCIATED WITH TRANSFORMING GROWTH-FACTOR-BETA-1 GROWTH-INHIBITION AND AUTOINDUCTION IN MCF-7 BREAST ADENOCARCINOMA CELLS

被引：20

作者：

LAFON, C ^{[1
]}

MAZARS, P ^{[1
]}

GUERRIN, M ^{[1
]}

BARBOULE, N ^{[1
]}

CHARCOSSET, JY ^{[1
]}

VALETTE, A ^{[1
]}

机构：

[1] CNRS, PHARMACOL & TOXICOL FONDAMENTALES LAB, F-31077 TOULOUSE, FRANCE

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 1995年 / 1266卷 / 03期

关键词：

TGF-BETA-1; AUTOINDUCTION; INHIBITION OF CELL PROLIFERATION; EARLY GENE RESPONSE; PROTEIN KINASE C; HUMAN BREAST ADENOCARCINOMA CELL;

D O I：

10.1016/0167-4889(95)00023-L

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In the human breast carcinoma cell Line (MCF-7), exogenous TGF-beta 1 induces a dose-dependent inhibition of cell proliferation. In a MCF-7 cell subline [MCF-7(-)], which has an undetectable level of type II TGF-beta receptor, exogenous TGF-beta 1 does not inhibit cell proliferation but is still able to induce its own message. In both cell lines, TGF-beta 1 stimulates expression of c-jun, whereas a rapid, transient and marked increase in c-fos mRNA is only observed in the MCF-7 cells sensitive to the growth inhibitory effect of TGF-beta 1. Depletion of protein kinase C abolishes the c-fos but not the c-jun response to TGF-beta 1. Our results suggest that growth inhibition and autoinduction by TGF-beta 1 are mediated by different signalling pathways. In addition, a PKC-dependent increase in c-fos expression seems to be associated with the growth inhibitory effect of TGF-beta 1.

引用

页码：288 / 295

页数：8

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