Objective: Long non-coding RNA LINC00173 (LINC00173) has been shown to facilitate the progression of a number of malignancies. In this study, we aimed to investigate the function of LINC00173 on prostate cancer (PCa) and discover the potential regulatory mechanism.
Patients and methods: RT-PCR was used to determine the levels of LINC00173, miR-338-3p and Rab25 in PCa patients and cell lines. The clinical significance of LINC00173 was statistically analyzed in 124 PCa patients. CCK-8, colony formation, transwell, scratch wound, Ethynyldeoxyuridine (EdU) assays and flow cytometry assays were used to detect the proliferation, apoptosis, invasion and migration of PCa cells. The mechanism of LINC00173 action was explored through bioinformatics, RNA pull-down assays and Luciferase reporter assays.
Results: We observed that the expression of LINC00173 and Rab25 was distinctly upregulated in both PCa specimens and cell lines, while miR-338-3p expression was significantly down-regulated. High LINC00173 expression was associated with Gleason score, preoperative PSA level and reduced patient survivals. Functional assays revealed that knockdown of LINC00173 suppressed the proliferation, migration and invasion of PCa cells, and promoted apoptosis. Mechanistically, LINC00173 acted as a competitive endogenous RNA in PCa and increased Rab25 expressions via sponging miR-338-3p. Moreover, LINC00173 promoted PCa progression by interacting with miR-338-3p and Rab25.
Conclusions: Our findings, for the first time, identified a novel PCa-related lncRNA, LINC00173 which might serve as an oncogene in PCa. The discovery of the LINC00173/miR-338-3p/Rab25 pathways provided new thinking for the treatments of PCa.