ABSTRACT
OBJECTIVES: To investigate the expression and mechanism of the long non-coding RNA (lncRNA) HCG22 in oral squamous cell carcinoma (OSCC). METHODS: HCG22 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. RESULTS: Compared 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). CONCLUSIONS: HCG22 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.
Subject(s)
Carcinoma, Squamous Cell , Head and Neck Neoplasms , MicroRNAs , Mouth Neoplasms , RNA, Long Noncoding , Carcinoma, Squamous Cell/genetics , Cell Line, Tumor , Cell Movement , Cell Proliferation , Gene Expression Regulation, Neoplastic , Humans , MicroRNAs/genetics , Mouth Neoplasms/genetics , RNA, Long Noncoding/genetics , Squamous Cell Carcinoma of Head and NeckABSTRACT
OBJECTIVE: To screen the genes related with leukocyte responses in mice early after burn injury by bioinformatic analysis of the gene expression profiling data. METHODS: The gene expression profiles were obtained from GEO (GSE7404, Mouse musculus, 25% TBSA, full-thickness) database. T test, fold changes and GO functional enrichment analysis were used to identify the differentially expressed genes (DEGs) related to leukocyte responses to burns; the interacting genes were transferred to STRING to construct the protein-protein interaction (PPI) network. Biological annotation of the sub-networks was executed using the software Cytoscape. Real-time PCR and Western blotting were used to verify the DEGs in mice. RESULTS: In mice at 1 day post-burn, a total of 658 genes were up-regulated and 1167 were down-regulated. PPI network and module analysis suggested that some of the genes (Stat1, Cdk1, Cd19, Lck and Jun) may play critical roles in the PPI network post-burn. Real-time PCR and Western blotting results in mice were consistent with those of bioinformatic analysis of Stat1, Cdk1 and Jun. CONCLUSION: Stat1, Cdk1 and Jun might be critical players in the development of leukocyte response in mice early after burn injury. Our finding provides new insights into the pathogenesis of leukocyte response to burn injury and identifies several biomarkers as potential targets for burn treatment.
