Fig. 4: PARK2 was regulated by miR and the BCL-XL can be a therapeutic target. | Cell Death & Disease

Fig. 4: PARK2 was regulated by miR and the BCL-XL can be a therapeutic target.

From: Suppressing BCL-XL increased the high dose androgens therapeutic effect to better induce the Enzalutamide-resistant prostate cancer autophagic cell death

Fig. 4

A qRT-PCR was performed to show quantification of PARK2 related miRs expression after 50 nM DHT treatment. B Western blotting shows BCL-XL and PARK2 expression after EnzR-C4-2 cells were treated with miR-493-3p inhibitor and 50 nM DHT. C Cell colony assay shows cell growth with 50 nM DHT when sh-miR-493-3p in EnzR-C4-2. D Potential AR response elements (AREs) were predicted on the miR-493 2.5 kb of 5’-promoter region (left). Chromatin immunoprecipitation (ChIP) binding assay was performed on EnzR-C4-2 cells (right). E The wild-type and mutant pGL3-miR-493 promoter-reporter constructs. F Luciferase activity after transfection of wild-type or mutant miR-493 promoter-reporter construct in EnzR-C4-2 cells with 50 nM DHT treatment. G The wild-type and mutant oe-PARK2 luciferase constructs. H Luciferase activity after transfection of wild-type or mutant PARK2 3’-UTR with 50 nM DHT treatment. Data are presented as means ± SD. *p < 0.05 was considered statistically significant by students’ t-test for two groups or ANOVA for more than two groups.

Back to article page