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. Author manuscript; available in PMC: 2019 May 15.
Published in final edited form as: Autophagy. 2019 Feb 20;15(5):886–899. doi: 10.1080/15548627.2019.1569912

Figure 2. Autophagy inhibition promotes oncogenic RAS-induced EMT.

Figure 2

(A) Immunofluorescence staining of LC3 (green), CDH1 (green), ZEB1 (red) or F-actin in HKe3 ER:HRAS V12 cells with the indicated treatments. Rhodamine-phalloidin was used to stain F-actin. TO-PRO-3 (blue) was used to stain nucleic acids. Scale bar: 20μm. (B) Protein expression of CDH1, ZEB1, SNAI2, SNAI1, ZEB2, TWIST1, ATG12–ATG5 and phospho-MAPK/ERK (p-MAPK) in HKe3 ER:HRAS V12 cells with the indicated treatments. TUBB was used as a loading control. (C) Fold change in mRNA levels of CDH1, ZEB1 and SNAI2 in HKe3 ER:HRAS V12 cells with the indicated treatments. mRNA levels normalized to ACTB/β-actin in control cells were used to set the baseline value at unity. Data are mean ± s.d. n = 3 samples per group. n.s. P > 0.05, *** P < 0.001. (D) Protein expression of CDH1, ZEB1, SNAI2 and ATG12–ATG5 in 4-OHT-treated HKe3 ER:HRAS V12 cells with the indicated treatments. TUBB was used as a loading control.