Y-H Bao1, Y Wang, Y Liu, S Wang, B Wu. 1. Department of Urology, General Hospital of Benxi Iron and Steel CO. LTD, Benxi, China. yuhaibaoio@163.com.
Abstract
OBJECTIVE: Previous studies showed that miR-96 was associated with a carcinogenic effect. To investigate the expression of miR-96 and related target genes in the regulation of prostatic cancer, we compared the expression of miR-96 in both prostatic cancer and adjacent normal tissues, and explored the role of miR-96 in prostate cancer. PATIENTS AND METHODS: PC-3 cell line originated from human prostatic cancer tissues was prepared. RNA was extracted for examination of miR-96 expression. The expressional alternation of miR-96 target genes, forkhead box O1 (FOXO1) and forkhead box O3a (FOXO3a), in prostatic cancer, was confirmed by PC-3 cells transfected with miR-96 and anti miR-96. RESULTS: Compared with control group, levels of FOXO1 and FOXO3a in PC-3 cells treated with anti miR-96 were 1.584 times and 1.637 times higher, respectively. Further, PC-3 cells were transfected with siRNA targeting FOXO1 and FOXO3a, resulting in a significant decrease of FOXO1 and FOXO3a expression, as verified by qPCR and Western blot analyses. Compared with untreated groups, proliferation and cell clonal formation exhibited a marked increase in PC-3 cells under transfection with both siR-FOXO1 and siR-FOXO3a. CONCLUSIONS: As target genes of miR-96, FOXO1 and FOXO3a confer protection against prostatic cancer, while the inhibition of FOXO1 and FOXO3a enhances cancer proliferation.
OBJECTIVE: Previous studies showed that miR-96 was associated with a carcinogenic effect. To investigate the expression of miR-96 and related target genes in the regulation of prostatic cancer, we compared the expression of miR-96 in both prostatic cancer and adjacent normal tissues, and explored the role of miR-96 in prostate cancer. PATIENTS AND METHODS: PC-3 cell line originated from humanprostatic cancer tissues was prepared. RNA was extracted for examination of miR-96 expression. The expressional alternation of miR-96 target genes, forkhead box O1 (FOXO1) and forkhead box O3a (FOXO3a), in prostatic cancer, was confirmed by PC-3 cells transfected with miR-96 and anti miR-96. RESULTS: Compared with control group, levels of FOXO1 and FOXO3a in PC-3 cells treated with anti miR-96 were 1.584 times and 1.637 times higher, respectively. Further, PC-3 cells were transfected with siRNA targeting FOXO1 and FOXO3a, resulting in a significant decrease of FOXO1 and FOXO3a expression, as verified by qPCR and Western blot analyses. Compared with untreated groups, proliferation and cell clonal formation exhibited a marked increase in PC-3 cells under transfection with both siR-FOXO1 and siR-FOXO3a. CONCLUSIONS: As target genes of miR-96, FOXO1 and FOXO3a confer protection against prostatic cancer, while the inhibition of FOXO1 and FOXO3a enhances cancer proliferation.