Rac1b Supports Ligand-Independent Androgen Receptor Activation in Prostate Cancer Progression

Author Info

Anke Augspach Stefanie Kowarschik Cordula A. Jilg Gudula Schmidt

Corresponding Author

Gudula Schmidt
Institute for Experimental and Clinical Pharmacology and Toxicology, Albert-Ludwigs-University of Freiburg, Freiburg im Breisgau, Germany

A B S T R A C T

Prostate cancer represents one of the leading causes of morbidity and mortality of men worldwide. In precision medicine, tumors are screened for specific genetic alterations known as predictive markers for targeted therapy. In androgen-independent prostate cancer cells and in tissue samples of a prostate cancer patient treated with Goserelin, we identified the self-activating splice variant Rac1b. Importantly, the expression of Rac1b was sufficient to induce AR-dependent gene synthesis. We hypothesized that Rac1b antagonizes androgen depletion induced cancer cell death by blocking pro-apoptotic signalling pathways. In line with that selective knockdown of Rac1b or inhibition of Rac-dependent signalling pathways reinduced apoptosis in androgen-independent prostate cancer cells suggesting Rac1b inhibition as a potential novel therapeutic add on strategy against prostate cancer.

Article Info

Article Type

Research Article

Publication history

Received: Thu 04, Jun 2020
Accepted: Thu 18, Jun 2020
Published: Tue 30, Jun 2020

Copyright

© 2023 Gudula Schmidt. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Hosting by Science Repository.
DOI: 10.31487/j.COR.2020.06.19