LINC00460 promotes pancreatic cancer progression by sponging miR‐491‐5p. (10th May 2021)

• Record Type: Journal Article
• Authors: Wu, Jiali; Sun, Shuxin; Liao, Wei; Chen, Enni; Wang, Xiaonan; Song, Yunda; Duan, Fangting; Deng, Wuguo; Li, Shengping
• Is Part Of: Journal of gene medicine. Volume 23:Number 6(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-05-10
• Subjects: LINC00460 -- miR‐491‐5p -- pancreatic cancer; Genetic transformation -- Periodicals; Gene Transfer -- Periodicals; Gene Therapy -- Periodicals; 616.042
• DOI: 10.1002/jgm.3333
• Languages: English
• ISSNs: 1099-498X

Abstract

Abstract: Background: A growing body of studies have suggested that LINC00460 is instrumental in tumorigenesis and tumour progression. Nonetheless, the biological function and mechanisms of LINC00460 in pancreatic ductal adenocarcinoma (PDAC) remain vague. Methods: Analysis based on public databases and a quantitative reverse transcription‐polymerase chain reaction were performed to screen for differentially expressed lncRNAs in PDAC and to detect LINC00460 expression in PDAC cell lines and clinical samples. The survival of patients in the up‐regulated and down‐regulated LINC00460 expression groups was compared by using the Kaplan–Meier method. In addition, the potential biological functions of LINC00460 in PDAC were explored by cell counting kit‐8, colony formation, flow cytometry and transwell assays. Furthermore, bioinformatics analysis, luciferase reporter assays and rescue experiments were applied to demonstrate the mechanism by which LINC00460 could directly bind to and inhibit miR‐491‐5p. Results: LINC00460 is up‐regulated in PDAC and correlates with adverse survival outcomes. The results of functional tests verified that LINC00460 knockdown inhibited both cell proliferation and cell migration. Additionally, knockdown led to G0/G1 cell cycle blockage and enhanced cell apoptosis. Mechanistic investigations revealed that LINC00460 directly binds to and attenuates the tumour suppressor miR‐491‐5p, thus accelerating PDAC progression. Conclusions: This research showed that LINC00460 is overexpressed in PDAC and correlates with adverse clinical outcomes. Additionally, LINC00460 promotes the aggressiveness of PDAC by targeting miR‐491‐5p. Thus, LINC00460 may serve as diagnostic biomarker of PDAC and a new target for PDAC therapy. Abstract : This research showed that LINC00460 is overexpressed in PDAC and correlates with adverse clinical outcomes. Additionally, LINC00460 promotes the aggressiveness of pancreatic ductal adenocarcinomas (PDAC) by targeting miR‐491‐5p. Thus, LINC00460 may serve as diagnostic biomarker of PDAC and a new target for PDAC therapy. ​