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. 2017 Dec 28;15(3):3305–3312. doi: 10.3892/ol.2017.7708

Figure 2.

Figure 2.

miR-433 accelerates acquired chemoresistance of gallbladder cancer cells by targeting cyclin M. (A) Putative miR-433-binding sequences in the 3′UTR of cyclin M (FAM58A) mRNA. (B) Relative expression of miR-433 in GR and non-GR subclones. (C) Relative luciferase activity in CycM WT 3′UTR (cells were transfected with pMIR-CycM-3′UTR) and CycM mut 3′UTR (cells were transfected with mut-pMIR-CycM-3′UTR)-293T cells. β-galactosidase activity was used as a normalization control. (D) Western blot analysis of cyclin M expression in GBC-SD cells following transfection with miR-433 or anti-miR-433. β-actin was used as a loading control. (E) Cell viability (expressed as a percentage) of GBC-SD cells following transfection with miR-433 or anti-miR-433 in response to 0.5 and 1 µg/ml gemcitabine. (F) Relative expression of miR-433 in supernatants from GR and non-GR subclones. (G) Relative expression of miR-433 in serum samples. Patients in the longer survival time group and shorter survival time group underwent chemotherapy with gemcitabine or 5-fluorouracil. The first samples were collected from the patients prior to receiving chemotherapy and the second samples were collected following three chemotherapy cycles. *P<0.05; **P<0.01. GR, gemcitabine-resistant; CDK10, cyclin-dependent kinase 10; 3′UTR, 3′ untranslated region; miR, microRNA; luc, luciferase; GBC, gallbladder cancer; CycM, cyclin M; WT, wild-type; mut, mutant; Co, transfected with the plasmids which contained CDK10-ORF and CycM-ORF.