Fig. 7

TSSC3 overexpression induces autophagy in osteosarcoma cells via inactivating the Src-mediated PI3K/Akt/mTOR pathway. a Representative images of the western blotting analysis of TSSC3, Src, p-Src, Akt, p-Akt, mTOR, and p-mTOR levels in MTF and SaOS2 cells. Cells were treated with or without TSSC3-overexpression. Protein levels on the western blots were quantified by densitometry of TSSC3, normalized to GAPDH and the levels of phosphorylated proteins were normalized to their total protein levels. Values are shown as fold change relative to the control (TSSC3-) groups. Quantification data was in Additional file 3: Figure S7a. b Representative images of the western blotting analysis of TSSC3, ATG5, P62, LC3, Src, Akt, mTOR and their phosphorylated versions in MTF and SaOS2 cells. Cells were treated with TSSC3-overexpression, IGF-1, p-YEEI, and BEZ235 separately or in combination. Protein levels on the western blots were quantified by densitometry of ATG5, LC3-II, and P62, normalized to GAPDH and the levels of phosphorylated proteins were normalized to their total protein levels. Values are shown as the fold change relative to the control groups. Quantification data was in Additional file 3: Figure S7b. c Schematic model illustrating how TSSC3 induces autophagy and the role of autophagy in the anti-tumor effect of TSSC3 in osteosarcoma