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Fig. 5 | Cell Communication and Signaling

Fig. 5

From: KLF4, a miR-32-5p targeted gene, promotes cisplatin-induced apoptosis by upregulating BIK expression in prostate cancer

Fig. 5

miR-32-5p inhibited KLF4 expression in prostate cancer cells. a Potential binding region of miR-32-5p on KLF4 was predicted by TargetScan. The sequences of KLF4 3’UTR containing the wild type miR-32-5p binding site or the mutant were constructed into a pSICHECK2 vector, where the red indicates the mutated region. b-d The wild type or mutant of KLF4 3’UTR was transfected into PC3 and DU145 cells with or without miR-32-5p overexpression. The luciferase activities were measured. The expression levels of KLF4 were detected by western blotting. Data represent the mean ± SD of three independent experiments. **p < 0.01 and ***p < 0.001 vs. control. e-f The KLF4 3’UTR was transfected into PC3 and DU145 cells with or without miR-32-5p inhibitor. The luciferase activities were measured. The expression levels of KLF4 were detected by western blotting. Data represent the mean ± SD of three independent experiments. **p < 0.01 vs. control. g-j The KLF4 3’UTR was transfected into PC3 and DU145 cells with or without miR-32-5p overexpression and then the cells were treated with 20 μM cisplatin at the indicated times. The luciferase activities were measured. The expression levels of KLF4 were detected by western blotting. Data represent the mean ± SD of three independent experiments. **p < 0.01 vs. control

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