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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 1. Autophagy inhibition promotes EMT in RAS-mutated cells.

Figure 1

(A) Protein expression of CDH1 and ATG12–ATG5 in the indicated pancreatic cancer cell lines transfected with control siRNA or ATG5 siRNA. TUBB/β1-tubulin was used as a loading control. For protein expression of CDH1 and ATG12–ATG5 in pancreatic cancer cell lines with mutant KRAS, both short and long exposures (respectively) are shown. KRAS mutation status is indicated under the blots. (B) Fold change in mRNA levels of CDH1, SNAI1, SNAI2, TWIST1, ZEB1 and ZEB2 in the indicated pancreatic cancer cell lines transfected with control siRNA or ATG5 siRNA. GAPDH-normalized mRNA levels in control cells were used to set the baseline value at unity. Data are mean ± s.d. n = 3 samples per group. * P < 0.05. ** P < 0.01. *** P < 0.001. (C) Immunofluorescence staining of CDH1 (green) in HRas V12-expressing Atg7+/+ tumors or HRas V12-expressing atg7-/- tumors. TO-PRO-3 (blue) was used to stain nucleic acids. Scale bar: 20 μm. Atg7+/+ or atg7-/- iBMK cells transduced with HRas V12 were subcutaneously injected in nude mice to form tumors. The graph shows the average relative intensity of CDH1 per cell evaluated using ImageJ, and data are mean ± s.d. n = 4 random fields. *** P < 0.001.