Long non‐coding <scp>RNA LINC01207</scp> promotes prostate cancer progression by downregulating <scp>microRNA</scp>‐1972 and upregulating <scp>LIM</scp> and <scp>SH3</scp> protein 1

Abstract

Prostate cancer is a heritable and clinically heterogeneous cancer. Both long non-coding RNAs (lncRNAs) and microRNAs (miRs) have been implicated in the pathogenesis and development of prostate cancer. Analysis of microarray data indicated that the lncRNA LINC01207 was differentially expressed in prostate cancer. In silico analysis predicted the interaction between LINC01207 and miR-1972 as well as the interaction between miR-1972 and the mRNAs LIM and SH3 protein 1 (LASP1). Thus, we explored the role of LINC01207 and miR-1972 in the growth and progression of prostate cancer. Quantitative real-time polymerase chain reaction revealed that LINC01207 and LASP1 were highly expressed in prostate cancer, while miR-1972 expression was lower. The interaction among LINC01207, miR-1972, and LASP1 was confirmed by RNA-fluorescence in situ hybridization, RNA immunoprecipitation, and dual luciferase reporter assay, which verified that LINC01207 could bind to miR-1972 and downregulate miR-1972, and miR-1972 targeted LASP1 and negatively regulated its expression. Both in vitro and in vivo experiments found that silencing LINC01207 inhibited cell proliferation, migration, invasion and tumor formation and enhanced apoptosis in prostate cancer cells, suggesting that LINC01207 functioned as a tumor promoter in prostate cancer and that it may represent a novel therapeutic target.