Regulation of Amphiregulin mRNA by TGF-beta in the Human Lung Adenocarcinoma Cell Line A549

被引：18

作者：

Bennett, Kelly L. ^{[1
]}

Plowman, Gregory D. ^{[1
]}

Buckley, Sharon D. ^{[1
]}

Skonier, John ^{[1
]}

Purchio, A. F. ^{[1
]}

机构：

[1] Bristol Myers Squibb, Seattle, WA 98121 USA

来源：

GROWTH FACTORS | 1992年 / 7卷 / 03期

关键词：

TCF-beta; AR; EGF; growth inhibition;

D O I：

10.3109/08977199209046925

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Transforming growth factor beta is a strong growth inhibitor for many types of normal and transformed cells, although little is known on the mechanism of this anti-proliferative effect. The human lung adenocarcinoma cell line A549 is growth arrested by TGF-beta 1 and serves as a model for studying this effect. We describe that, concurrent with the inhibition of A549 cell growth, TGF-beta 1 treatment causes a dramatic reduction in the level of expression of the amphiregulin (AR) gene, a recently identified member of the EGF/TGF alpha family. Similar results were also observed with TGF-beta 2. Peak inhibition occurred at 24 hr of treatment and was reversible upon removal of TGF-beta 1. The level of AR protein secreted by A549 cells was also decreased by TGF-beta 1. In contrast, TGF-alpha mRNA was not detected in these cells regardless of TGF-beta 1 treatment. Another TGF-beta inhibited cell line, PC-3 (human prostatic adenocarcinoma) also exhibited a decrease in AR message levels following exposure to TGF-beta 1. The growth inhibitory effects of TGF-beta may in part be mediated by modulation of AR expression.

引用

页码：207 / 213

页数：8

共 50 条

[1]

ASSOIAN RK, 1983, J BIOL CHEM, V258, P7155

[2]

ASSOIAN RK, 1984, CELL, V36, P35, DOI 10.1016/0092-8674(84)90071-0

[3]

ASSOIAN RK, 1985, J BIOL CHEM, V260, P9613

[4] THE CELL BIOLOGY OF TRANSFORMING GROWTH-FACTOR-BETA [J].