Fig. 3: miR-34a/b/c-deficiency increases EBSS- and Tunicamycin-induced autophagic flux, while ectopic expression of miR-34a inhibits autophagy. | Cell Death & Differentiation

Fig. 3: miR-34a/b/c-deficiency increases EBSS- and Tunicamycin-induced autophagic flux, while ectopic expression of miR-34a inhibits autophagy.

From: CRISPR/Cas9-mediated inactivation of miR-34a and miR-34b/c in HCT116 colorectal cancer cells: comprehensive characterization after exposure to 5-FU reveals EMT and autophagy as key processes regulated by miR-34

Fig. 3

A Cells were incubated in complete medium or EBSS for 24 h. 20 μM of chloroquine was added for the last 4 h before Western blot analyses of the indicated proteins. B Cells stably expressing GFP-LC3-RFP were incubated in complete medium or EBSS for 24 h and then subjected to FACS analysis. C WT and miR-34a/b/c-KO cells were treated with DMSO or Tunicamycin for 24 h. 20 μM of chloroquine was added for the last 4 h before Western blot analyses of the indicated proteins. D FACS analysis of cells stably expressing GFP-LC3-RFP treated with DMSO or Tunicamycin for 24 h. E Doxycycline was added as indicated to induce ectopic expression of miR-34a in SW480 cells. 20 μM of chloroquine was added for the last 4 h before Western blot analyses of the indicated proteins. Results are presented as the mean ± SD (n = 3) for B and D with *p < 0.05.

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