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Long non‐coding RNA LINC01207 promotes prostate cancer progression by downregulating microRNA ‐1972 and upregulating LIM and SH3 protein 1
Author(s) -
Wang Sugui,
Qiu Jianguo,
Wang Liping,
Wu Ziyu,
Zhang Xianyun,
Li Qiang,
Jiang Fujin
Publication year - 2020
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.2327
Subject(s) - prostate cancer , microrna , gene silencing , cancer research , biology , downregulation and upregulation , cancer , microarray analysis techniques , microbiology and biotechnology , gene expression , gene , genetics
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.