Fig. 6: Effects of the miR-135b–BMAL1 axis on chemoresistance of PC cells. | Cell Death & Disease

Fig. 6: Effects of the miR-135b–BMAL1 axis on chemoresistance of PC cells.

From: The MiR-135b–BMAL1–YY1 loop disturbs pancreatic clockwork to promote tumourigenesis and chemoresistance

Fig. 6

a, b Concentration-dependent inhibition of cell viability in response to gemcitabine (GEM) in MIA PaCa-2 or Panc-1 cells stably transfected with corresponding vectors. c–f Xenograft models were used to test the in vivo relevance of the miR-135b–BMAL1 axis and GEM resistance. Equal amounts of miR-135b and/or BMAL1-manipulated MIA PaCa-2 cells (c, d) or Panc-1 cells (e, f) were subcutaneously implanted on the back-side of each nude mouse. GEM treatment began at day 0. Tumour volume was monitored every 4 days (d, f). Mice were killed at the end of day 20 and xenografts were excised, photographed and weighed (c, e). g Representative dot-plots illustrating the apoptotic status of MIA PaCa-2 or Panc-1 cells using Annexin V-FITC/ PI method. Cells were treated with different doses of GEM (0, 1 or 5 μmol/L). The dot-plots in the right upper quadrant (Q2) and the right lower quadrant (Q3) were quantified as the percentage of apoptotic cells. Histograms indicated the proportion of cell apoptosis in MIA PaCa-2 (h) and Panc-1 cells (i). *P < 0.05. (j) Expression of the apoptosis-related proteins was detected by western blotting after a 72 h-exposure to GEM (1 μmol/L for MIA PaCa-2; 5 μmol/L for Panc-1). β-actin was used as internal control protein

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