Fig. 1

Superoxide anions potentiate mTORC2 signaling. a Pyrogallol treated MDA-MB-231 cells exhibited elevated mTORC2-specific markers, pSer²⁴⁸¹-mTOR, pSer⁴⁷³-AKT, and pSer⁶⁵⁷-PKC-α. b Four different cell lines viz. MDA-MB-231, DU 145, PC-3, and MCF7 exhibited increased mTORC2 signaling following Pyrogallol (20 μM) treatment for 24 h. c Attenuation of mTORC2 cascade via Rictor directed siRNA resulted in diminished pSer²⁴⁸¹-mTOR, pSer⁴⁷³-AKT, and pSer⁶⁵⁷-PKC-α despite Pyrogallol (20 μM) treatment. d The in vitro kinase assay showing mTORC2 immunopurified from Pyrogallol treated MDA-MB-231 cells exhibited elevated kinase activity as compared to mTORC2 purified from non-treated cells. e Pre-treatment with mitochondria permeating superoxide anion quencher MnTBAP attenuated Pyrogallol (20 μM) stimulated mTORC2 signaling. f Modulating superoxide anion levels indirectly by gene-based downregulation/upregulation of mitochondrial resident SOD2 resulted in potentiated/attenuated mTORC2 signaling respectively. All data are representative of three independent experiments. ns, not significant. *P ≤ 0.05, **P ≤ 0.01 and ***P ≤ 0.001