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Long noncoding RNA LINC00460 promotes carcinogenesis via sponging miR‐613 in papillary thyroid carcinoma
Author(s) -
Feng Li,
Yang Bin,
Tang XiaoDi
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27799
Subject(s) - gene knockdown , cancer research , downregulation and upregulation , biology , long non coding rna , carcinogenesis , cell growth , thyroid carcinoma , metastasis , cancer , cell culture , endocrinology , thyroid , gene , biochemistry , genetics
Abstract Long intergenic noncoding RNA 460 (LINC00460) has been identified as a critical regulator for multiple types of cancers. However, the biological role and underlying mechanism in human papillary thyroid carcinoma (PTC) still remain unclear and need to be uncovered. This study was aimed to ascertain the biological role and molecular mechanism of LINC00460 in PTC progression. Our findings revealed that the level of LINC00460 was significantly upregulated in PTC tissues and cell lines, which was positively correlated with advanced tumor–node–metastasis (TNM) stage and lymph node metastasis. Cellular experiments exhibited that knockdown of LINC00460 decreased proliferative, migratory, and invasive abilities of PTC cells. Mechanism assays noted that knockdown of LINC00460 suppressed cell proliferation, migration, and invasion, and inhibited expression of sphingosine kinase 2 (SphK2, a target of miR‐613) in PTC cells, at least in part, by regulating miR‐613. These findings suggested that LINC00460 could function as a competing endogenous RNA to regulate SphK2 expression by sponging miR‐613 in PTC. Targeting LINC00460 could be a promising therapeutic strategy for patients with PTC.