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Long noncoding RNA LINC00339 promotes laryngeal squamous cell carcinoma cell proliferation and invasion via sponging miR‐145
Author(s) -
Liu Shouzhou,
Duan Wenchao
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28110
Subject(s) - gene silencing , cell growth , gene knockdown , cancer research , oncogene , biology , cell , downregulation and upregulation , long non coding rna , epithelial–mesenchymal transition , microrna , cell culture , cell cycle , gene , genetics
Laryngeal squamous cell carcinoma (LSCC) is a very common neoplasm of the head and neck in the world. Long noncoding RNAs play key roles in cell infiltration, fate, apoptosis, and invasion. However, the functional role and expression of LINC00339 remains unclear in LSCC. In this study, we showed that the expression level of LINC00339 was upregulated in LSCC tissues and cell lines. LINC00339 silencing suppressed the proliferation, invasion, and epithelial‐mesenchymal transition (EMT) progression of LSCC cells. In addition, we showed that LINC00339 acted as a sponge of miR‐145, and LINC00339 silencing promoted the expression of miR‐145 in Hep2 cell. Furthermore, the expression of miR‐145 was lower in LSCC tissues than in their paired normal samples and the miR‐145 expression level was negatively correlated with LINC00339 expression in LSCC tissues. The knockdown of miR‐145 promoted the proliferation, invasion, and EMT progression of LSCC cells. Finally, we indicated that LINC00339 silencing inhibited the proliferation, invasion, and EMT progression of LSCC cells by suppressing the miR‐145 expression. These data suggested that LINC00339 acted as an oncogene in the development of LSCC, partly by regulating the miR‐145 expression.