Overexpression of miR-518b in non-small cell lung cancer serves as a biomarker and facilitates tumor cell proliferation, migration and invasion

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Abstract

Several microRNAs (miRNA/miR) have been reported to serve critical roles in tumorigenesis. The present study aimed to investigate miR-518b expression in non-small cell lung cancer (NSCLC), and determine its clinical significance and biological function in this malignancy. Reverse transcription-quantitative PCR was performed to assess miR-518b expression in NSCLC. The diagnostic value of miR-518b was determined via a receiver operating characteristic curve, while its prognostic value was assessed using the Kaplan-Meier method. Gain- and loss-of-function experiments were performed to determine the functional role of miR-518b in NSCLC progression. The results demonstrated that miR-518b expression was upregulated in NSCLC serum, tissues and cell lines compared with the corresponding normal controls. Furthermore, high miR-518b expression was significantly associated with larger tumor size, lymph node metastasis and advanced TNM stage, as well as poor overall survival in patients with NSCLC. Serum miR-518b expression was identified as a candidate diagnostic biomarker for NSCLC, with sensitivity of 88.1% and specificity of 81.7%. Furthermore, the cell experiments indicated that NSCLC cell proliferation, migration and invasion were enhanced following overexpression of miR-518b; however, these effects were reversed following miR-518b knockdown. Taken together, the results of the present study suggest that elevated miR-518b expression in NSCLC serves a potential oncogenic role by facilitating tumor cell proliferation, migration and invasion, and thus may serve as a candidate diagnostic and prognostic biomarker.

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Zhang, X., Hu, Y., Gong, C., & Zhang, C. (2020). Overexpression of miR-518b in non-small cell lung cancer serves as a biomarker and facilitates tumor cell proliferation, migration and invasion. Oncology Letters, 20(2), 1213–1220. https://doi.org/10.3892/ol.2020.11667

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