1. SH3GL2 translocation to mitochondria induces ROS production and modulates mitochondria function.
SH3GL2 translocation to mitochondria induces ROS production and modulates mitochondria function. A, SH3GL2-overexpressing breast cancer cells produced significantly higher amount of superoxides (P = –0.0003), exhibited an enhanced expression of CYTC in the cytoplasm compared with mitochondria (B), and demonstrated increased numbers of mitochondrial fusion bodies compared with the empty vector–treated cells (C). D and E, enhanced expression of MFN2, PINK1, and MT-TFA in the whole-cell or mitochondrial lysate of the SH3GL2-transduced groups compared with the empty vector–treated groups. EV, empty vector transduced; SH3GL2, SH3GL2-transduced cells. β-Actin and IMMT were used as cytosolic and mitochondrial loading controls. F, confocal imaging demonstrating colocalization of GFP-tagged SH3GL2 and MitoTracker Red–labeled mitochondria in MDA-MB-231 cells. Scale bar, 50 μm; magnification, 200× (A) and 400× (C and F). G, confocal imaging showing colocalization of endogenous SH3GL2 and mitochondria in the naïve MDA-MB-231 cells (arrowheads). Scale bar, 20 μm; magnification, 400×.
Anbarasu Kannan et al. Clin Cancer Res 2016;22:
©2016 by American Association for Cancer Research