Silencing LINC00491 inhibits prostate cancer development through the miR‐384/TRIM44 axis

• Published in: Journal of biochemical and molecular toxicology Vol. 37; no. 7; pp. e23370 - n/a
• Main Authors: Zhou, Songlin, Wu, Cheng, Tang, Qingsheng, Zhou, Xunrong, He, Bin, Chang, Pingan, He, Xiaozhou
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.07.2023
• Subjects: Bioinformatics; Biomarkers; Carcinogenesis; Cell growth; Cell Line, Tumor; Cell Movement; Cell Proliferation; Fractionation; Gene Expression Regulation, Neoplastic; Humans; Intracellular Signaling Peptides and Proteins - genetics; LINC00491; Male; MicroRNAs - metabolism; miR‐384; Molecular modelling; Polymerase chain reaction; Prostate cancer; Prostatic Neoplasms - metabolism; Prostatic Neoplasms - pathology; Reporter gene; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Tissues; TRIM44; Tripartite Motif Proteins - genetics; Tripartite Motif Proteins - metabolism; Tumor cell lines; Tumorigenesis; Tumors; prostate cancer; miR-384; LINC00491; TRIM44
• ISSN: 1095-6670; 1099-0461
• DOI: 10.1002/jbt.23370

Accumulating evidence has demonstrated the key role of long noncoding (lnc)RNAs in tumorigenesis. Prostate cancer (PCa) is a cancer with high mortality that requires further exploration of the underlying molecular mechanisms. In the present study, we aimed to discover novel potential biomarkers for diagnosing PCa and targeting treatment. Overexpression of the lncRNA, LINC00491, was verified in PCa tumor tissues and cell lines using the real‐time polymerase chain reaction. Cell proliferation and invasion were then analyzed via the Cell Counting Kit‐8, colony formation, and transwell assays in vitro, and tumor growth in vivo. The interaction of miR‐384 with LINC00491, as well as TRIM44, was investigated via bioinformatics analyses, subcellular fractionation, luciferase reporter gene assays, radioimmunoprecipitation, pull‐down, and western blot analyses. LINC00491 was overexpressed in PCa tissues and cell lines. LINC00491 knockdown resulted in impaired cell proliferation and invasion in vitro and decreased tumor growth in vivo. Moreover, LINC00491 acted as a sponge for miR‐384 and its downstream target, TRIM44. Additionally, miR‐384 expression was downregulated in PCa tissues and cell lines, and its expression was negatively correlated with LINC00491. A miR‐384 inhibitor restored the inhibitory effects of LINC00491 silencing on PCa cell proliferation and invasion. LINC00491 is a tumor promoter in PCa via enhancing TRIM44 expression by sponging miR‐384 to facilitate the development of PCa. LINC00491 plays a significant role in PCa and could serve as both a biomarker for early diagnosis and a novel treatment target.