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Long non‐coding RNA LOC554202 promotes laryngeal squamous cell carcinoma progression through regulating miR‐31
Author(s) -
Yang Shujuan,
Wang Jing,
Ge Wensheng,
Jiang Yanfang
Publication year - 2018
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.26902
Subject(s) - cell growth , cell cycle , cell , oncogene , ectopic expression , biology , flow cytometry , cancer research , microrna , microbiology and biotechnology , gene , genetics
Laryngeal squamous cell carcinoma (LSCC) is one aggressive malignancy and accounts for 20% of all head and neck cancer. However, the role of LOC554202 in human LSCC remains unknown. The expression level of LOC554202 and miR‐31 was detected in the LSCC tiussues by using qRT‐PCR. Cell growth was measured by CCK‐8 assay. Flow cytometry and matrigel‐coated membrane was used to detect for cell cycle and invasion respectively. We indicated that lncRNA LOC554202 expression was overexpressed in LSCC tissues compared with the paired adjacent samples and higher LOC554202 expression was associated with the advanced stage. In addition, we demonstrated that the expression level of miR‐31 was downregulated in LSCC tissues compared to the paired adjacent samples and lower miR‐31 expression was correlated with the advanced stage. Moreover, the expression of miR‐31 was negatively correlated with the expression of LOC554202 in LSCC tissues. Ectopic expression of LOC554202 promoted LSCC cell growth, cell cyle and cell invasion and overexpression of miR‐31 inhibited LSCC cell growth, cell cyle and cell invasion. Elevated expression of LOC554202 suppressed miR‐31 expression and promoted RhoA expression in LSCC cell, which was a direct target gene of miR‐31. Furthermore, LOC554202 increased LSCC cell growth, cell cyle and cell invasion through suppressing miR‐31 expression. These results suggested that LOC554202 acted as an oncogene in the development of LSCC.