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Long noncoding RNA H19 competitively binds miR‐17‐5p to regulate YES 1 expression in thyroid cancer
Author(s) -
Liu Lin,
Yang Jian,
Zhu Xuchao,
Li Dan,
Lv Zhongwei,
Zhang Xiaoping
Publication year - 2016
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.13741
Subject(s) - competing endogenous rna , gene knockdown , cancer research , microrna , carcinogenesis , biology , ectopic expression , oncogene , thyroid cancer , long non coding rna , downregulation and upregulation , rna binding protein , cancer , cell growth , rna , cell cycle , cell culture , gene , genetics
The long noncoding RNA H19 is overexpressed in many cancers and acts as an oncogene. Here, we investigated the role of H19 in thyroid carcinogenesis and its relation to micro RNA miR‐17‐5p and its target gene YES 1. H19 expression was higher in tumor samples and in thyroid cancer cell lines than nontumor tissues and normal thyroid cells. H19 knockdown and ectopic expression in the TPC ‐1 and NIM thyroid cancer cell lines showed that overexpression of H19 promoted proliferation, migration, and invasion, whereas H19 knockdown reduced cell viability and invasion and induced growth arrest in vitro and in vivo . H19 was identified as a target of miR‐17‐5p, by Dual‐Luciferase Reporter assays and RNA ‐binding protein immunoprecipitation assays. H19 antagonized the function of miR‐17‐5p on upregulation of its target YES 1 and inhibited miR‐17‐5p‐induced cell cycle progression. Our results suggest that H19 functions as a competitive endogenous RNA (ce RNA ) by acting as a sink for miR‐17‐5p, revealing a potential ce RNA regulatory network involving H19 and miR‐17‐5p with a role in the modulation of YES 1 expression. This mechanism may contribute to a better understanding of thyroid cancer pathogenesis and provide new insights into the treatment of this disease.