Effect and Mechanism of lncRNA CERS6-AS1 on the Biological Behavior of Prostate Cancer Cell

Objective. To investigate the effect of long noncoding RNA (lncRNA) CERS6 antisense RNA1 (CERS6-AS1) on the biological behavior of prostate cancer cells DU145 and its mechanism. Methods. RT-PCR was used to detect the relative level of CERS6-AS1 and miR-16-5p in prostate cancer tissues, adjacent tissues, prostate cancer cells DU145, and human normal prostate epithelial cells RWPE-1. DU145 cells were divided into control group, si-CERS6-AS1 group, si-NC group, miR-16-5p mimic group, miR-NC group, and si-CERS6-AS1+miR-16-5p inhibitor group. And CCK-8 method and colony formation test was applied to detect cell proliferation ability, flow cytometry was selected to calculate cell apoptosis, and scratch healing test was employed to assess cell migration ability. Western blot was determined to detect high mobility protein A2 (HMGA2) expression. RT-PCR and dual-luciferase reporter experiments were used to analyze the targeting relationship among CERS6-AS1, miR-16-5p, and HMGA2. Results. Compared with the adjacent tissues, the relative level of CERS6-AS1 in prostate cancer tissue was increased (P < 0.05), and the relative level of miR-16-5p was decreased (P < 0.05). Compared with RWPE-1 cells, the relative level of CERS6-AS1 in DU145 cells was increased (P < 0.05), and the relative level of miR-16-5p was decreased (P < 0.05). Compared with the control group and the si-NC group, the HMGA2 protein expression, the colony formation number, and the scratch healing rate of DU145 cells in the si-CERS6-AS1 group and the miR-16-5p mimic group were reduced (P < 0.05), and the relative level of miR-16-5p and the proliferation inhibition rate and apoptosis were increased (P < 0.05). miR-16-5p is specifically bound to CERS6-AS1 and HMGA2, respectively. Compared with the si-CERS6-AS1 group, the HMGA2 protein expression, the colony formation number, and the scratch healing rate of DU145 cells in the si-CERS6-AS1+miR-16-5p inhibitor group were increased (P < 0.05), and the cell proliferation inhibition rate and apoptosis rate were reduced (P < 0.05). Conclusion. Silencing CERS6-AS1 can inhibit the proliferation and migration of prostate cancer cell DU145 and induce cell apoptosis, the mechanism is related to the regulation of the miR-16-5p/HMGA2 axis.

Automated summary

Silencing CERS6-AS1 can inhibit the proliferation and migration of prostate cancer cells DU145 and induce cell apoptosis, and the mechanism may be related to the regulation of the miR-16-5p/HMGA2 axis.