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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 microRNA miR-17–5p and its target gene YES1. 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 YES1 and inhibited miR-17–5p-induced cell cycle progression. Our results suggest that H19 functions as a competitive endogenous RNA (ceRNA) by acting as a sink for miR-17–5p, revealing a potential ceRNA regulatory network involving H19 and miR-17–5p with a role in the modulation of YES1 expression. This mechanism may contribute to a better understanding of thyroid cancer pathogenesis and provide new insights into the treatment of this disease.We report a potential role for the long noncoding RNA H19 as a competitive endogenous RNA (ceRNA) in thyroid cancer. We found that H19 promotes proliferation, migration, and invasion of thyroid cancer cells in vitro and in vivo. This protumorigenic effect of H19 is linked to its ability to bind and sequester miR-17–5p, which in turn derepresses YES1 expression.