Targeted deletion of Smad4 shows it is required for transforming growth factor β and activin signaling in colorectal cancer cells

被引：119

作者：

Zhou, SB

Buckhaults, P

Zawel, L

Bunz, F

Riggins, G

Dai, JL

Kern, SE

Kinzler, KW

Vogelstein, B

机构：

[1] Johns Hopkins Univ, Sch Med, Ctr Oncol, Johns Hopkins Oncol Ctr, Baltimore, MD 21231 USA

[2] Johns Hopkins Univ, Howard Hughes Med Inst, Baltimore, MD 21231 USA

[3] Johns Hopkins Univ, Dept Pathol, Baltimore, MD 21205 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1998年 / 95卷 / 05期

关键词：

D O I：

10.1073/pnas.95.5.2412

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Smad4 (DPC4) is a candidate tumor suppressor gene that has been hypothesized to be critical for transmitting signals from transforming growth factor (TGF) beta and related ligands. To directly test this hypothesis, the Smad4 gene was deleted through homologous recombination in human colorectal cancer cells. This deletion abrogated signaling from TGF-beta, as well as from the TGF-beta family member activin. These results provide unequivocal evidence that mutational inactivation of Smad4 causes TGF-beta unresponsiveness and provide a basis for understanding the physiologic role of this gene in tumorigenesis.

引用

页码：2412 / 2416

页数：5

共 56 条

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