C-Y Hu1, P You, J Zhang, H Zhang, N Jiang. 1. Department of Urology, Gongli Hospital Affiliated to The Second Military Medical University, Shanghai, China. sh_huchuanyi@tom.com.
Abstract
OBJECTIVE: Researches have indicated that microRNA-506-3p (miR-506-3p) was downregulated and functioned as tumor suppressor in cancers. However, the biological role of miR-506-3p in prostate cancer (PCa) remains to be elucidated. MATERIALS AND METHODS: Expression of miR-506-3p in PCa cell lines was measured by qRT-PCR. Effects of miR-506-3p expression on PCa cell behaviors were investigated with MTT assay, colony formation assay, and transwell invasion assay. Connection of miR-506-3p and N-Acetylgalactosaminyltransferase-4 (GALNT4) was analyzed with luciferase activity reporter assay and Western blot assay. RESULTS: miR-506-3p expression was downregulated in PCa cell lines. Function studies demonstrated that overexpression of miR-506-3p inhibits PCa tumor progression in vitro. Mechanistic investigations found GALNT4 was a direct target of miR-506-3p. Overexpression of GALNT4 reversed the tumor-suppressive effects of miR-506-3p on PCa cell. CONCLUSIONS: Our results elucidated genetic silencing of miR-506-3p enhances GALNT4 oncogene expression to accelerate PCa progression.
OBJECTIVE: Researches have indicated that microRNA-506-3p (miR-506-3p) was downregulated and functioned as tumor suppressor in cancers. However, the biological role of miR-506-3p in prostate cancer (PCa) remains to be elucidated. MATERIALS AND METHODS: Expression of miR-506-3p in PCa cell lines was measured by qRT-PCR. Effects of miR-506-3p expression on PCa cell behaviors were investigated with MTT assay, colony formation assay, and transwell invasion assay. Connection of miR-506-3p and N-Acetylgalactosaminyltransferase-4 (GALNT4) was analyzed with luciferase activity reporter assay and Western blot assay. RESULTS:miR-506-3p expression was downregulated in PCa cell lines. Function studies demonstrated that overexpression of miR-506-3p inhibits PCa tumor progression in vitro. Mechanistic investigations found GALNT4 was a direct target of miR-506-3p. Overexpression of GALNT4 reversed the tumor-suppressive effects of miR-506-3p on PCa cell. CONCLUSIONS: Our results elucidated genetic silencing of miR-506-3p enhances GALNT4 oncogene expression to accelerate PCa progression.