1. Academic Validation
  2. miR‑490‑5p regulates the proliferation, migration, invasion and epithelial‑mesenchymal transition of pharyngolaryngeal cancer cells by targeting mitogen‑activated protein kinase kinasekinase 9

miR‑490‑5p regulates the proliferation, migration, invasion and epithelial‑mesenchymal transition of pharyngolaryngeal cancer cells by targeting mitogen‑activated protein kinase kinasekinase 9

  • Int J Mol Med. 2019 Jul;44(1):240-252. doi: 10.3892/ijmm.2019.4196.
Arikin Abdeyrim 1 Xiuqin Cheng 1 Meng Lian 2 Yuanyouan Tan 1
Affiliations

Affiliations

  • 1 Department of Otorhinolaryngology Head and Neck Surgery, The People's Hospital of Xinjiang Uygur Autonomous Region, Ürümqi, Xinjiang 830001, P.R. China.
  • 2 Department of Otorhinolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing 100005, P.R. China.
Abstract

MicroRNA (miRNA/miR) has been identified to be a promising tool in treating pharyngolaryngeal Cancer. The present study aimed to investigate the role of miR‑490‑5p in the regulation of proliferation, migration, invasion and epithelial‑mesenchymal transition (EMT) of pharyngolaryngeal Cancer cells. The data of miR‑490‑5p expression levels of 45 cases were obtained from the People's Hospital of Xinjiang Uygur Autonomous Region, and the prediction of the target of miR‑490‑5p was conducted by bioinformatics and verified using a luciferase assay. Cell viability was determined by cell counting kit‑8. Migration and invasion rates were measured by wound healing test and Transwell apparatus, respectively. Colony formation rate was measured by plate colony formation assay. mRNA and protein levels were determined by quantitative polymerase chain reaction and western blotting, respectively. miR‑490‑5p expression was significantly depressed in primary pharyngolaryngeal Cancer tissues and cell lines, leading to an unfavorable prognosis. Evidently, miR‑490‑5p overexpression decreased the cell viabilities of BICR 18 and FaDu cells. Mechanically, miR‑490‑5p could target mitogen‑activated protein kinase kinasekinase 9 (MAP3K9). The overexpression of MAP3K9 could promote cell viability, migration and invasion rates, EMT process and ability of cloning, miR‑490‑5p could target MAP3K9 and further modulate the proliferation, migration, invasion and EMT of pharyngolaryngeal Cancer cells. The results of the present study provide a novel entry point to the treatment of pharyngolaryngeal Cancer.

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