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. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: Cancer Res. 2015 Feb 17;75(7):1388–1398. doi: 10.1158/0008-5472.CAN-14-2561

Figure 4. Overexpression of miR26a prevents Fat-1-induced inhibition of cholangiocarcinoma growth in vitro.

Figure 4

Different groups of CCLP1 cells (Fat-1 expression, miR26a overexpression, Fat-1/miR26a co-expression and control) were analyzed for cell proliferation by WST-1 assay and by colony formation assay. (A) Overexpression of Fat-1 inhibited CCLP1 colony forming ability; this effect was reversed by overexpression of miR-26a. Overexpression of miR26a alone was found to enhance CCLP1 colony formation efficiency. Representative of three independent experiments were showed in upper panel. Quantified results were normalized to control group and presented as mean±SE in lower panel; *P<0.05; **P<0.01; (B) Overexpression Fat-1 inhibited CCLP1 growth in vitro; this effect was reversed by miR26a overexpression. Overexpression miR26a alone significantly enhanced CCLP1 growth. The data are presented as mean±SE from 3 independent experiments. **P<0.01; (C) The levels of 15-PGDH protein in CCLP1 cells with Fat-1 overexpression, miR26a overexpression, Fat-1/miR26a co-expression, or control vector cells. Total protein was analyzed by Western blot with 15-PGDH antibody. β-actin were measured as a reference gene.