Abstract
Abstract Our laboratory has previously characterized a microRNA, miR-3189-3p, with potent anti-cancer activity against glioblastoma and triple negative breast cancer (TNBC), two of the most aggressive types of tumors. Intriguingly, while miR-3189-3p inhibits proliferation, migration, and invasion of glioblastoma and TNBC cells, it does not induce apoptosis. The BCL2 family of proteins controls mitochondrial-mediated cell death through binding affinity and abundance of pro- and anti-apoptotic factors. Here, we investigated the mechanisms of the cytostatic effect of miR-3189-3p on MDA-MB-231 cells and found that the BCL2-family members and pro-apoptotic factors BAK1, BMF, and HRK, which are predicted gene target of this miRNA, are indeed downregulated by the miRNA mimic. In addition, we found that expression of miR-3189-3p improved the metabolic fitness of TNBC cells through increasing both mitochondrial respiration and glycolysis. Ongoing experiments are aimed at understanding how changes in the metabolic profile and cytostatic activity of miR-3189-3p could be used for therapeutic intervention against this aggressive tumor. Citation Format: Cecilia Vittori, Hassan Yousefi, Krzysztof Reiss, Francesca Peruzzi. The cytostatic effect of miR-3189-3p in triple negative breast cancer cells involves inhibition of mitochondrial-mediated apoptosis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1545.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.