Fig. 3 | Scientific Reports

Fig. 3

From: Transcriptional regulation of ETV5 by mitogen-activated protein kinase via ETS-1 in human pancreatic cancer cells

Fig. 3

Effects of ETV5 knockdown by small interfering RNAs on human pancreatic cancer cell lines. (A) Alterations in ETV5 expression at the mRNA level measured by qRT-PCR in pancreatic cancer cells treated with si#1, small interfering RNAs for ETV5, and siNC, small interfering RNAs for a negative control. (B) A representative immunoblot showing the expression of pERK, ETV5 and β-actin in pancreatic cancer cells with knockdown of ETV5 (si#1) or a negative control (siNC). Original blots are shown in Supplemental Figure S2. (C and D) Densitometry analyses of immunoblots probed for the expression of pERK, ETV5 and β-actin in pancreatic cancer cells with knockdown of ETV5 (si#1) or a negative control (siNC). (E) MTT assays for proliferations of pancreatic cancer cells with knockdown of ETV5 (si#1) or a negative control (siNC). (F) Scratch wound healing assays for migration of pancreatic cancer cells with knockdown of ETV5 (si#1) or a negative control (siNC). (G) The graph shows the rate of closing of the wound area in each pancreatic cancer cell line. (H) Chemosensitivity assays for gemcitabine in pancreatic cancer cells. The chemosensitivity was assessed as relative amount of siRNA (either si#1 for ETV5 (black lines) or siNC for negative control (gray lines)) transfected viable cells of gemcitabine-treated compared to amount of viable cells of the control without siRNA transfection and gemcitabine treatment in average of those of 5-wells at each time point. Abbreviations: n.s., not significant. Asterisks indicate *, p < 0.05; **, p < 0.01; and ***, p < 0.001. Scale bars in Fig. 3D indicate 100 μm. Graphs show means and standard errors obtained from duplicate experiments unless otherwise specified.

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