Therapeutic targeting of the focal adhesion complex prevents oncogenic TGF-beta signaling and metastasis.

ABSTRACT:

Introduction

Mammary tumorigenesis is associated with the increased expression of several proteins in the focal adhesion complex, including focal adhesion kinase (FAK) and various integrins. Aberrant expression of these molecules occurs concomitant with the conversion of TGF-beta function from a tumor suppressor to a tumor promoter. We previously showed that interaction between beta3 integrin and TbetaR-II facilitates TGF-beta-mediated oncogenic signaling, epithelial-mesenchymal transition (EMT), and metastasis. However, the molecular mechanisms by which the focal adhesion complex contributes to beta3 integrin:TbetaR-II signaling and the oncogenic conversion of TGF-beta remain poorly understood.

Methods

FAK expression and activity were inhibited in normal and malignant mamma

SUBMITTER: Wendt MK 

PROVIDER: S-EPMC2790843 | biostudies-literature | 2009

REPOSITORIES: biostudies-literature