ObjectiveTo investigate the expression and mechanism of the long non-coding RNA (lncRNA) HCG22 in oral squamous cell carcinoma (OSCC).
MethodsHCG22 levels were detected in the OSCC and adjacent tissues, OSCC cells, and normal oral keratinocytes. HCG22 expression in SCC-25 and HSC-3 cells was upregulated by transfection of the overexpressing plasmi dvector. Methyl thiazolyl tetrazolium (MTT) assay, flow cytometry, and Transwell assay were employed to detect changes in cell proliferation, apoptosis, migration, and invasion ability, while Western blotting was used to detect the expression of epithelial-mesenchymal transformation-related proteins. The expression level of miR-650 in the cells was detected by real-time quantitative polymerase chain reaction (RT-qPCR), and dual-luciferase reporter gene assay was applied to assess the targeting relationship between HCG22 and miR-650.
ResultsCompared with that in adjacent tissues, the expression of HCG22 significantly decreased in OSCC tissues (P<0 .05). moreover, the prognostic survival of patients in the low-hcg22 expression group was significantly lower than that in the high-expression group (P<0 .05). compared with that in hok cells, the expression of hcg22 was significantly lower in scc-25, hn13, hsc-3, and cal-27 cells (P<0 .05). upregulation of hcg22 expression could inhibit the proliferation, migration, invasion, and apoptosis of scc-25 and hsc-3 cells, upregulatethe expression of e-cadherin, and downregulate the expression of n-cadherin and vimentin (P<0 .05). mir-650 mimics could reduce the luciferase activity of hcg22 wild-type plasmid cells (P<0 .05), and the expression of mir-650 in scc-25 and hsc-3 cells decreased after upregulation of hcg22 expression (P<0 .05).
ConclusionHCG22 is expressed at low levels in OSCC. Upregulation of the expression of this lncRNA can inhibit the proliferation, migration, invasion, and epithelial-mesenchymal transition of OSCC cells. The mechanism of action of HCG22 may be related to its targeted regulation of miR-650.
