MiR-137 and its target TGFA modulate cell growth and tumorigenesis of non-small cell lung cancer

X. Liu, L. Chen, X.-D. Tian, T. Zhang

Department of Thoracic Surgery, Chinese PLA General Hospital, Haidian, Beijing, China. smlie3370@yeah.net

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• Oncology

OBJECTIVE: MiR-137 has been reported to serve as a tumor suppressor in non-small cell lung cancer (NSCLC). However, the potential mechanism remains largely unclear. The present study aimed to explore the potential molecular mechanisms by which miR-137 regulated NSCLC.

MATERIALS AND METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to quantify the expression levels of miR-137 in NSCLC tissues and cell lines. Dual-luciferase reporter assay was employed to confirm the specificity of miR-137 target genes. An MTT assay and flow cytometry were used to determine the rates of cell proliferation and cell cycle distribution. Furthermore, the effect of miR-137 up-regulation on TGFA expression was examined by western blot.

RESULTS: miR-137 expression levels in NSCLC cell lines or tissue were significantly lower than in a normal human lung cell line or adjacent normal tissues. We further found that upregulation of miR-137 inhibited the proliferation of NSCLC cells, whereas silencing of miR-137 promoted the proliferation of NSCLC. Moreover, we identified TGFA as a direct target gene of miR-137 in NSCLC cell. Finally, Similarly, knockdown of TGFA led to the suppression of NSCLC cell proliferation.

CONCLUSIONS: Overall, our findings indicated that miR-137 served as a tumor suppressor in NSCLC and its suppressive effect is mediated by repressing TGFA expression.

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