Figure 3. The Gαh-PLC-δ1 axis promotes autophagosome degradation in TNBC cells. (A) Results from the Western blot analysis for LC3-I/II, p62 and GAPDH proteins derived from the indicated TNBC cell lines. (B) Correlation of mRNA expression levels of Gαh and the autophagy-related gene set in a panel of breast cancer cell lines derived from the Cancer Cell Line Encyclopedia (CCLE) database. Spearman’s correlation test was used to estimate the statistical significance. (C–E) Results from the Western blot analysis of the LC3-I/II, p62 and GAPDH proteins derived from the parental (PT) HCC1806 cells without (vector control, VC) or with Gαh overexpression (C) and the parental MDA-MD231 cells without (nonsilenced, NS) or with Gαh knocked down using two independent shRNA clones (D), and MDA-MD231 cells treated without or with 10 μM Gαh/PLC-δ1 protein-protein interaction (PPI) inhibitor for 2 hours (E). In A, C, D, E, GAPDH was used as an internal control of protein loading. The protein intensities of representative blots from three independent experiments were normalized by GAPDH levels and presented as a ratio to the control group.