Abstract B27: Superoxide anion O2.-mediated activation of mTORC2 by estrogen receptor in breast cancer cells: Role of acetylation dependent inhibition of MnSOD

Conclusion: Our finding unravel a new role of MnSOD as important control switch through which ER might affect its downstream non genomic signaling cascades in a redox dependent manner particularly potentiation of mTOR signaling complex 2. We present data in support of MnSOD being responsible for previously reported ER dependent superoxide anion O2.- potentiation in breast cancer cells following E2 exposure. We showed that MnSOD interacts with ER alpha which in turn is associated with its diminished SIRT 3 dependent deacetylation, leading to its inhibition and superoxide anion O2.- build up and consequent activation of mTORC2Note: This abstract was not presented at the conference.Citation Format: Mehraj U din Lone, Ranjana Km Kanchan, Chakrapani Tripathi, Khemraj Singh Baghel, Brijnath Tiwari, Smrati Bhadauria. Superoxide anion O2.-mediated activation of mTORC2 by estrogen receptor in breast cancer cells: Role of acetylation dependent inhibition of MnSOD. [abstract]. In: Proceedings of the AACR Special Conference: Targeting the PI3K-mTOR Network in Cancer; Sep 14-17, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(7 Suppl):Abstract nr B27.
Source: Molecular Cancer Therapeutics - Category: Cancer & Oncology Authors: Tags: PI3K-mTOR Activation in Human Cancer: Poster Presentations - Proffered Abstracts Source Type: research