Fig. 6: UBE2O induced proliferation, EMT and CSPs in a manner dependent on the regulation of the UBE2O/AMPKα2/mTORC1 axis in BC. | Cell Death & Disease

Fig. 6: UBE2O induced proliferation, EMT and CSPs in a manner dependent on the regulation of the UBE2O/AMPKα2/mTORC1 axis in BC.

From: UBE2O promotes the proliferation, EMT and stemness properties of breast cancer cells through the UBE2O/AMPKα2/mTORC1-MYC positive feedback loop

Fig. 6

a Western blotting revealed that p-Raptor expression was increased in MDA-MB-231sh-UBE2O#1cells, which indicated mTORC1 pathway inhibition. As a downstream effector of mTORC1, p-S6K expression was also decreased. The opposite results occurred in MCF-7OE-UBE2O cells. bf AMPKα2 was knocked down in MDA-MB-231sh-NC/MDA-MB-231sh-UBE2O#1cells. Then, b scratch assays, c invasion assays, d colony formation assays, e CCK-8 assays and f sphere formation assays were performed (upper: magnification × 100, Scale bar, 100 μm; lower: magnification × 400, Scale bar, 20 μm). g Western blot assays were performed to detect the expression of EMT markers (CDH1, CDH2, vimentin and slug), CS markers (CD44, ABCG2, OCT3/4 and MYC) and mTORC1 pathway-related markers (p-Raptor and p-S6K) after AMPKα2 suppression in MDA-MB-231sh-NC/MDA-MB-231sh-UBE2O#1cells. The data are shown as the mean ± s.d. Student’s t test was used for statistical analysis: *p < 0.05, **p < 0.01, ***p < 0.001. The data represent at least three independent experiments.

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