Open AccessMiR-338-3p inhibits cell migration and invasion in human hypopharyngeal cancer via downregulation of ADAM17
Author(s) -
Yuchen Hong,
Xiaofang Chen,
Zhiyong Liang,
Zhihui Xu,
Yahong Li,
YiCong Pan
Publication year - 2020
Publication title -
anti-cancer drugs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.651
H-Index - 93
eISSN - 1473-5741
pISSN - 0959-4973
DOI - 10.1097/cad.0000000000000919
Subject(s) - wnt signaling pathway , microrna , cancer research , sox2 , downregulation and upregulation , hypopharyngeal cancer , homeobox protein nanog , cancer , biology , cell migration , nasopharyngeal carcinoma , cancer cell , signal transduction , microbiology and biotechnology , cell , medicine , gene , embryonic stem cell , genetics , induced pluripotent stem cell , radiation therapy
Studies have confirmed that microRNAs play important roles in the development and progression of cancer. Therefore, to identify the differentially expressed microRNAs between the cancer and the normal tissues, microRNAs will provide new clues for exploring the molecular mechanisms of cancer development and potential targeted therapies. In the present study, we found that miR-338-3p was downregulated in hypopharyngeal carcinoma and inversely correlated with the pathological grade. When the miR-338-3p was further downregulated, the migration and invasion ability of the FaDu hypopharyngeal carcinoma cells were enhanced, and these functions were inhibited when the miR-338-3p was upregulated. In addition, we demonstrated that ADAM17 was a target of miR-338-3p, and that ADAM17 directly activated the wnt/β-catenin signaling pathway and promoted the expression of its target gene MMP2, Nanog and SOX2, which affected the growth, migration and invasion of hypopharyngeal carcinoma cells. In conclusion, our results demonstrate for the first time that miR-338-3p targets ADAM17 and blocks the development of hypopharyngeal carcinoma involving the wnt/β-catenin signaling pathway, which may be a new target for clinical intervention in human cancer.