Article
Mutant FOXL2C134W Hijacks SMAD4 and SMAD2/3 to Drive Adult Granulosa Cell Tumors.
Cancer research - 1 Sept 2020
Weis-Banke Stine E, Lerdrup Mads, Kleine-Kohlbrecher Daniela, Mohammad Faizaan, Sidoli Simone, Jensen Ole N, Yanase Toshihiko, Nakamura Tomoko, Iwase Akira, Stylianou Anthe, Abu-Rustum Nadeem R, Aghajanian Carol, Soslow Robert, Da Cruz Paula Arnaud, Koche Richard P, Weigelt Britta, Christensen Jesper, Helin Kristian, Cloos Paul A C
Abstract excerpt
The mutant protein FOXL2C134W is expressed in at least 95% of adult-type ovarian granulosa cell tumors (AGCT) and is considered to be a driver of oncogenesis in this disease. However, the molecular mechanism by which FOXL2C134W contributes to tumorigenesis is not known. Here, we show that mutant FOXL2C134W acquires the ability to bind SMAD4, forming a FOXL2C134W/SMAD4/SMAD2/3 complex that binds a novel hybrid DNA...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.