Long noncoding RNA LINC00958 promotes the oral squamous cell carcinoma by sponging miR-185-5p/YWHAZ

• Published in: Life sciences (1973) 2020-02, Vol.242, p.116782-116782, Article 116782
• Main Authors: Wang, Zongsheng, Zhu, Xuemei, Dong, Pengfei, Cai, Jun
• Format: Article
• Language: English
• Subjects: Apoptosis; Assaying; Blotting, Western; Carcinoma, Squamous Cell - metabolism; Carcinoma, Squamous Cell - pathology; Cell Line, Tumor; Cell proliferation; Cholecystokinin; Female; Flow Cytometry; Gene Expression Regulation, Neoplastic; Humans; LINC00958; Male; MicroRNAs - metabolism; Middle Aged; miR-185-5p; Mouth Neoplasms - metabolism; Mouth Neoplasms - pathology; Oral squamous cell carcinoma; Polymerase chain reaction; Real-Time Polymerase Chain Reaction; Ribonucleic acid; RNA; RNA, Long Noncoding - physiology; Squamous cell carcinoma; Therapeutic applications; Tumorigenesis; Tumors; Western blotting; Xenografts; Xenotransplantation; YWHAZ
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2019.116782

Increasing evidence has indicated the essential roles of long noncoding RNA (lncRNA) in the oral squamous cell carcinoma (OSCC). However, there are still numerous uncertain mechanisms for the pathophysiological process of OSCC. In this work, we tried to identify the biological function and potential mechanism of lncRNA LINC00958 in the OSCC. The expressions of RNA and protein were measured by quantitative real-time polymerase chain reaction (RT-qPCR) and western blotting. The tumor behavior was detected using the CCK-8 assay, transwell assay, flow cytometry assay and xenograft in vivo assay. The interaction within LINC00958/miR-185-5p/YWHAZ was identified using the luciferase reporter assay. LINC00958 expression was remarkably up-regulated in the OSCC tissue and cell lines. Clinical investigation showed that LINC00958 overexpression was associated with poor prognosis, acting as an independent prognostic factor for OSCC. Loss- and gain-of-function assays indicated that LINC00958 promoted the proliferation, invasion and reduced the apoptosis of OSCC cells in vitro. In vivo, knockdown of LINC00958 repressed the tumor growth. Mechanistically, bioinformatic tools and luciferase reporter assay indicated that miR-185-5p both targeted the 3′-UTR of LINC00958 and YWHAZ, constructing the LINC00958/miR-185-5p/YWHAZ regulatory axis. Taken together, the findings in this research reveal the modulation of LINC00958 for the OSCC tumorigenesis through the miR-185-5p/YWHAZ axis, which might be useful for the mechanical investigation associated with OSCC therapeutic target.