A kinase-inactive type II TGFβ receptor impairs BMP signaling in human breast cancer cells

Abstract

Dominant negative receptor mutants are often utilized in order to abrogate signaling induced by growth factors. We have previously shown that expression of a dominant negative type II TGFβ receptor (dnTβRII) in MDA-MB-231 breast cancer cells effectively abrogates TGFβ signaling. In this letter, we report that expression of dnTβRII also impairs BMP2-mediated Smad1 phosphorylation as well as BMP2-mediated Smad-dependent transcriptional responses, resulting in an attenuation of BMP-mediated anti-proliferative effects. The fact that dnTβRII not only abrogates TGFβ signaling but BMP signaling as well has important implications for the interpretation of data in which dominant negative mutants are utilized.