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
收藏
页码：207 / 213
页数：8
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