MiR-1275 promotes non-small cell lung cancer cell proliferation and metastasis by regulating LZTS3 expression

J. He, L. Yu, C.-M. Wang, X.-F. Zhou

Department of Pneumology, the First Affiliated Hospital of Chengdu Medical College, Chengdu, China. qq157110097@aliyun.com

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• Oncology

OBJECTIVE: To detect the expressions of micro-ribonucleic acid 1275 (miR-1275) in non-small cell lung cancer (NSCLC) tissues and cells, analyze the correlations of the expression of miR-1275 with the clinicopathological features of NSCLC, and explore its biological function and potential molecular mechanism.

PATIENTS AND METHODS: Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to detect the relative expression levels of miR-1275 in NSCLC tissues and cells. The correlations of miR-1275 expression with clinicopathological features of NSCLC were statistically analyzed. Clone formation assay, flow cytometry and transwell assay were used to detect the effects of interfering in miR-1275 expression on biological behaviors of NSCLC cells. Bioinformatics was used to predict the downstream target genes of miR-1275, and qRT-PCR and Western blotting were utilized for verification. Dual luciferase reporter gene assay was used to validate the binding of miR-1275 to its target gene.

RESULTS: The results of qRT-PCR showed that among 70 cases of tissues from NSCLC patients, 52 cases had up-regulated miR-1275 expressions. MiR-1275 expression was increased in NSCLC cells compared with that in 16 human bronchial epithelial (16HBE) cells. Interfering in miR-1275 expression could inhibit the proliferation, invasion and metastasis of NSCLC cells. Bioinformatics prediction discovered that leucine zipper putative tumor suppressor 3 (LZTS3) might be a target gene of miR-1275. Dual luciferase reporter assay confirmed that the two genes could bind directly.

CONCLUSIONS: MiR-1275 is relatively highly expressed in NSCLC. Highly expressed miR-1275 can promote the proliferation and metastasis of NSCLC through regulating the expression of LZTS3.

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