MicroRNA-138 inhibits proliferation and induces apoptosis of laryngeal carcinoma via targeting MAPK6

Y.-H. Zhou, Y.-Y. Huang, M. Ma

Department of Otolaryngology, The 1st Affiliated Hospital of Henan University of Science and Technology, Henan, China. 39758242@qq.com

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• Oncology

OBJECTIVE: To explore whether microRNA-138 could regulate the incidence and progression of laryngeal carcinoma through modulating proliferation and apoptosis of laryngeal carcinoma cells via MAPK6.

PATIENTS AND METHODS: MicroRNA-138 expression in laryngeal carcinoma tissues and paracancerous tissues were detected by qRT-PCR (Quantitative Real-Time Polymerase Chain Reaction). The regulatory effects of microRNA-138 on proliferation and apoptosis of laryngeal carcinoma cells were detected by colony formation assay and flow cytometry, respectively. Target gene of microRNA-138 was predicted by online software and verified by luciferase reporter gene assay. Corresponding plasmids of microRNA-138 and the target gene were constructed. Rescue experiments were conducted to explore the regulatory effect of microRNA-138 on the target gene.

RESULTS: MicroRNA-138 was downregulated in laryngeal carcinoma tissues than that of paracancerous tissues. MicroRNA-138 knockdown resulted in increased proliferation and decreased apoptosis of laryngeal carcinoma cells. MAPK6 was predicted as the target gene of microRNA-138. Luciferase reporter gene assay further verified that MAPK6 could directly bind to microRNA-138. Both mRNA and protein levels of MAPK6 were downregulated after microRNA-13 overexpression in laryngeal carcinoma cells. Rescue experiment results indicated that increased proliferation and decreased apoptosis of laryngeal carcinoma cells resulted from microRNA-13 knockdown were partially reversed by MAPK6 overexpression.

CONCLUSIONS: MicroRNA-138 is downregulated in laryngeal carcinoma patients. MicroRNA-138 knockdown promotes proliferation and inhibits apoptosis of laryngeal carcinoma cells via inhibiting MAPK6 expression.

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