LncRNA linc00460 sponges miR-1224-5p to promote esophageal cancer metastatic potential and epithelial-mesenchymal transition

•LncRNA linc00460 was significantly up-regulated in both ESCA tissues and five cell lines.•Knockdown of Linc00460 suppressed cell metastatic potential (migration and invasion) and epithelial-mesenchymal transition (EMT) of ESCA.•Linc00460 may function as a molecular sponge to adsorb miR-1224-5p, the...

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Veröffentlicht in:Pathology, research and practice research and practice, 2020-07, Vol.216 (7), p.153026, Article 153026
Hauptverfasser: Cui, Yuanbo, Zhang, Chunyan, Lian, Hongkai, Xie, Linsen, Xue, Jinhui, Yin, Ningwei, Guan, Fangxia
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Sprache:eng
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Zusammenfassung:•LncRNA linc00460 was significantly up-regulated in both ESCA tissues and five cell lines.•Knockdown of Linc00460 suppressed cell metastatic potential (migration and invasion) and epithelial-mesenchymal transition (EMT) of ESCA.•Linc00460 may function as a molecular sponge to adsorb miR-1224-5p, thereby promoting ESCA metastasis and EMT. Increasing studies highlight the crucial role of long non-coding RNAs (lncRNAs) in carcinogenesis of various human cancer types, including esophageal cancer (ESCA). Long intergenic non-coding RNA 00460 (Linc00460), a novel oncogenic lncRNA, has been reported to accelerate ESCA cell growth. This study aimed to investigate the role and possible regulatory mechanism of linc00460 in ESCA metastasis. Bioinformatics analysis and quantitative real time polymerase chain reaction (qRT-PCR) were used to detect linc00460 expression in ESCA. Wound healing assay, Transwell assay and Western blot were utilized to examine migration, invasion and epithelial-mesenchymal transition (EMT) of ESCA cells. The direct binding effect between linc00460 and microRNA-1224-5p (miR-1224-5p) was evaluated by the dual luciferase reporter assay. In this study, we discovered that lncRNA linc00460 was obviously over-expressed in ESCA, both in tissues and cell lines. Down-regulation of linc00460 significantly suppressed the metastatic potential (including cell migration and invasion) and EMT of ESCA cells. In addition, miR-1224-5p, a potential tumor suppressor, was negatively correlated with linc00460 in ESCA. Linc00460 and miR-1224-5p could bind directly in ESCA cells. Inhibition of miR-1224-5p partially abrogated the effects of linc00460 decrease on metastatic potential and EMT of ESCA cells. Taken together, linc00460 may function as a molecular sponge to adsorb miR-1224-5p, thereby promoting ESCA metastasis and EMT. Our findings suggest that linc00460/miR-1224-5p is a possible clinical target for ESCA.
ISSN:0344-0338
1618-0631
DOI:10.1016/j.prp.2020.153026