SNHG1 promotes proliferation, invasion and EMT of prostate cancer cells through miR-195-5p.

Abstract

OBJECTIVE: To explore the correlation of SNHG1 with miR-195-5p, and the mechanism of SNHG1 in prostate cancer (PC). PATIENTS AND METHODS: The prostate cancer patients admitted to our hospital were selected, and the cancer tissues (n=142) and adjacent tissues (n=142) of the patients were collected during the operation. The content of SNHG1 and miR-195-5p in PC was observed, and the PC cell lines were transfected to detect the proliferation, invasion, apoptosis and Epithelial-Mesenchymal Transitions (EMT) capability. RESULTS: SNHG1 was enhanced in PC, while miR-195-5p was decreased (p<0.05). After transfection of DU-145 and PC-3, it was found that silence of SNHG1 or overexpression of miR-195-5p could evidently inhibit the proliferation and invasion, increase the apoptosis (p<0.05). After detecting the EMT markers, it was found that after silencing SNHG1 or over-expressing miR-195-5p, E-cadherin enhanced while N-cadherin and Vimentin reduced (p<0.05). Double Luciferase reports confirmed that SNHG1 could act as a sponge to regulate miR-195-5p, and correlation analysis showed that SNHG1 had a negative correlation with miR-195-5p. Rescue experiments found that si-SNHG1 co-transfected with miR-195-5p-inhibitor could reverse the inhibitory role of si-SNHG1 on prostate cancer cells. CONCLUSIONS: SNHG1 can mediate the proliferation, invasion and EMT of PC by regulating miR-195-5p expression.