RECK controls breast cancer metastasis by modulating a convergent, STAT3-dependent neoangiogenic switch.

ABSTRACT: Metastasis is the primary cause of cancer-related death in oncology patients. A comprehensive understanding of the molecular mechanisms that cancer cells usurp to promote metastatic dissemination is critical for the development and implementation of novel diagnostic and treatment strategies. Here we show that the membrane protein RECK (Reversion-inducing cysteine-rich protein with kazal motifs) controls breast cancer metastasis by modulating a novel, non-canonical and convergent signal transducer and activator of transcription factor 3 (STAT3)-dependent angiogenic program. Neoangiogenesis and STAT3 hyperactivation are known to be fundamentally important for metastasis, but the root molecular initiators of these phenotypes are poorly understood. Our study identifies loss of RECK as a critic

SUBMITTER: Walsh LA 

PROVIDER: S-EPMC4344427 | biostudies-literature | 2015 Apr

REPOSITORIES: biostudies-literature