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Linc00210 enhances the malignancy of thyroid cancer cells by modulating miR‐195‐5p/IGF1R/Akt axis
Author(s) -
Du Peijie,
Liu Fei,
Liu Yanling,
Shao Mingwei,
Li Xialian,
Qin Guijun
Publication year - 2020
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.29016
Subject(s) - downregulation and upregulation , cancer research , protein kinase b , pi3k/akt/mtor pathway , insulin like growth factor 1 receptor , malignancy , biology , nasopharyngeal carcinoma , cancer , long non coding rna , cell growth , signal transduction , microbiology and biotechnology , medicine , gene , growth factor , genetics , receptor , radiation therapy
Emerging evidence has indicated that long noncoding RNA (lncRNAs) play crucial roles in regulating thyroid cancer (TC) development. Linc00210 is a newly identified lncRNA which plays an oncogenic role in hepatocellular carcinoma and nasopharyngeal carcinoma, but whether Linc00210 can modulate the development of TC remains elusive. Here, we found that Linc00210 expression was upregulated in TC tissues compared to the matched noncancerous tissues. Overexpression of Linc00210 augmented the proliferation, migration, and invasion of TC cells. Mechanistically, Linc00210 served as a sponge for miR‐195‐5p, thereby counteracting its ability in downregulating the expression of IGF1R and the activation of PI3K/Akt signaling. Moreover, inhibition of Linc00210 suppressed the growth of TC cells in nude mice. Our findings for the first time uncovered the oncogenic property of Linc00210 in TC.