miRNA‑375 regulates the cell survival and apoptosis of human non‑small cell carcinoma by targeting HER2.

Longqiang Cheng, Bingxiang Zhan, Peng Luo, Baolong Wang

Molecular medicine reports 2017 Mar

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micro (mi)‑RNAs are a class of small non‑coding RNAs that regulate gene expression by binding to the 3'‑untranslated region of mRNA, which may lead to mRNA degradation or transcription regulation. Previous studies indicated that miRNAs are important for the pathogenesis of human cancer. miR‑375 has been implicated in various tumor types; however, the biological activity in human non‑small cell lung carcinoma (NSCLC) cells remains to be fully elucidated. The purpose of the present study was to investigate the biological importance of miR‑375 in human NSCLC cells. The expression of miRNAs and mRNA was determined using reverse transcription‑quantitative polymerase chain reaction. Cell proliferation was analyzed using a Cell Counting kit‑8 assay. Cell apoptosis was analyzed using a fluorescence‑activated cell sorting assay. The migration and invasion abilities of cells were evaluated using an in vivo mouse model. Dual‑luciferase assay and western blotting were used to determine the potential target of miR‑375. The results indicated that the expression of miR‑375 in human NSCLC cells was significantly downregulated and induction of miR‑375 may inhibit the proliferation of human NSCLC cells by inducing apoptosis. An animal model was used to determine that the upregulation of miR‑375 inhibited the migration and invasion of A549 human NSCLC cells in vivo. It was also determined that human epidermal growth factor receptor 2 (HER‑2) was a direct target gene of miR‑375 and induction of miR‑375 may reduce the expression of HER‑2 in human NSCLC cells. These findings suggested that miR‑375 may act as a potential therapeutic target for human NSCLC cancer in the future.

Citation

Longqiang Cheng, Bingxiang Zhan, Peng Luo, Baolong Wang. miRNA‑375 regulates the cell survival and apoptosis of human non‑small cell carcinoma by targeting HER2. Molecular medicine reports. 2017 Mar;15(3):1387-1392