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MicroRNA‐103 promotes nasopharyngeal carcinoma through targeting TIMP‐3 and the Wnt/β‐catenin pathway
Author(s) -
Zhao Yigang,
Gu Xiao,
Wang Yanpeng
Publication year - 2020
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1002/lary.28045
Subject(s) - wnt signaling pathway , cyclin d1 , nasopharyngeal carcinoma , viability assay , cancer research , microrna , carcinogenesis , catenin , medicine , mtt assay , ectopic expression , downregulation and upregulation , cell growth , microbiology and biotechnology , cell , biology , cell culture , signal transduction , cell cycle , cancer , gene , genetics , radiation therapy
Objectives/Hypothesis To verify how microRNA‐103 (miR‐103) is involved in nasopharyngeal carcinoma (NPC) development. Study Design Research on the relationship between miR‐103 and NPC. Methods Tissue inhibitor of metalloproteinases‐3 (TIMP‐3) was identified as the theoretical target gene of miR‐103, and its regulatory mechanism in NPC was explored by quantitative reverse transcription polymerase chain reaction, Western blot, MTT, transwell, and luciferase reporter assays. Results MiR‐103 was upregulated whereas TIMP‐3 was markedly decreased in NPC tissue samples. Ectopic expression of miR‐103 promoted NPC cell viability, migration, and invasion. In vitro assay showed that TIMP‐3 recovered miR‐103–mediated promotion of NPC cell viability, migration, and invasion. The expression of Wnt/β‐catenin pathway markers (β‐catenin and cyclin D1) were enhanced after miR‐103 overexpression. Conclusions MiR‐103 might play a key role in NPC carcinogenesis by targeting TIMP‐3 and affecting the Wnt/β‐catenin pathway. Level of Evidence NA Laryngoscope , 130:E75–E82, 2020