Long non-coding RNA MIR503HG serves as a tumor suppressor in non-small cell lung cancer mediated by wnt1

H. Lin, P. Li, N. Zhang, L. Cao, Y.-F. Gao, F. Ping

Department III of Geriatrics, Hebei General Hospital, Shijiazhuang, China. 13932123573@126.com

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• Oncology

OBJECTIVE: The incidence and death rate of lung cancer has been rising year by year. Non-small cell lung cancer (NSCLC) seriously affects people’s health and quality of life. This study was designed to explore the functional role of long-chain non-coding RNA (LncRNA) MIR503HG in the development of NSCLC.

PATIENTS AND METHODS: The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay was conducted to access the expression level of MIR503HG in NSCLC cell lines and tissues. The Cell Counting Kit-8 (CCK-8) assay, colony formation assay, and flow cytometric analysis were performed to assess the ability of MIR503HG in regulating cell proliferation and apoptosis in NSCLC. Subsequently, Western blotting was used to detect the expression level of Wnt1 in NSCLC. Besides, in vivo tumorigenesis assay was performed in nude mice to examine the ability of MIR503HG in tumor formation.

RESULTS: MIR503HG was downregulated in NSCLC. CCK-8 assay and colony formation assay revealed that MIR503HG negatively regulated cell proliferation in NSLCL progression. In addition, MIR503HG promoted cell apoptosis and suppressed cell cycle progression in NSCLC in vitro. MIR503HG inhibited tumor formation in nude mice bearing NSCLC in vivo. MIR503HG downregulated Wnt1 expression in NSCLC.

CONCLUSIONS: Lon non-coding RNA MIR503HG was downregulated in NSCLC. The over-expression of MIR503HG suppressed cell proliferation and promoted cell apoptosis in vitro and repressed tumorigenesis in vivo. MIR503HG suppressed NSCLC progression via negatively regulating Wnt1 expression.

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