Microarray profile of circular RNAs identifies hsa_circRNA_102459 and hsa_circRNA_043621 as important regulators in oral squamous cell carcinoma.

Circular RNAs (circRNAs) have emerged as important regulators of carcinogenesis. However, the role of circRNAs in oral squamous cell carcinoma (OSCC) remains limited. Here, total RNAs were extracted from three pairs of OSCC and adjacent normal tissues and subjected to circRNA microarrays to detect the differentially expressed circRNAs. Gene Ontology (GO) and functional category analyses were used to identify circRNAs associated with tumor cell proliferation pathways. Then, gain­of­function assays or loss­of­function assays were conducted to investigate the functions of the most upregulated and downregulated circRNAs on TSCC1 cell proliferation, cell cycle and apoptosis using CCK­8 and EdU assays, flow cytometry and Hoechst 33258 staining, respectively. The results revealed that hsa_circRNA_102459 was significantly downregulated and hsa_circRNA_043621 was significantly upregulated in OSCC tissues. Clinical stage, tumor differentiation, lymph node metastasis presented significant difference in regards to the expression of circRNA_043621 and circRNA_102459. The in vitro experiments further demonstrated that upregulation of circRNA_102459 or downregulation of circRNA_043621 significantly suppressed TSCC1 cell proliferation, induced cell cycle G0/G1 phase arrest and promoted apoptosis. Furthermore, the MAPK and PI3K/Akt pathways were suppressed, while Bcl­2 family members were activated by circRNA_102459 overexpression and circRNA_043621 knockdown. Taken together, our study indicates that differentially expressed circRNAs are closely related to the carcinogenesis of OSCC. Among these, circRNA_102459 and circRNA_043621 may function as a tumor­suppressor and promoter, respectively, of OSCC carcinogenesis, and thus may be valuable diagnostic biomarkers of OSCC.

Knockdown of IFI27 inhibits cell proliferation and invasion in oral squamous cell carcinoma.

BACKGROUND: The development of oral squamous cell carcinoma (OSCC) involves genetic mutations, epigenetic gene expression modification, and other processes. It has been reported that IFI27 is upregulated in OSCC, but its function is unknown. The aim of this study was to investigate the role of IFI27 on OSCC cell proliferation and invasion. METHODS: The protein level of IFI27 in OSCC tissues and adjacent tissues was detected by immunohistochemistry. In the OSCC cell model, we designed the IFI27 siRNA to downregulate the expression of IFI27; gene and protein of IFI27 in those models were then detected by Q-PCR and Western blot. MTT assay was used to detect the effect of -IFI27 knockdown on cell proliferation; Annexin V-PI staining flow cytometry was used to detect the effect of IFI27 downregulation on apoptosis of cancer cells. The effect of IFI27 downregulation on oral cancer cell invasion was detected using Transwell assay. RESULTS: IFI27 was highly expressed in OSCC tissues by immunohistochemical assay. In the OSCC cell model, IFI27 siRNA could downregulate the mRNA and protein expression level of IFI27. As showed in MTT assay, Annexin V-PI assay, and Transwell assay, through the downregulation of IFI27, TSCCA and TCA8113 cell proliferation were inhibited, OSCC cell apoptosis was promoted, and its migration and invasion were inhibited. CONCLUSION: IFI27 is involved in the development and progression of OSCC. Its high expression promotes cell proliferation and invasion and reduces apoptosis. These findings may provide new biomarkers and therapeutic targets for OSCC diagnosis and clinical treatment.

[Association of pleomorphic adenoma gene 1 polymorphism and benign parotid tumor in Chinese Han population in Hainan Province].

OBJECTIVE: To investigate the relationship between rs6474051 polymorphism of pleomorphic adenoma gene 1 (PLAG1) and the benign parotid tumor in Chinese Han population in Hainan Province. METHODS: Sixty-five patients with benign parotid tumor and 69 healthy volunteers (control) were examined for Rs6474051 polymorphisms of PLAG1 gene by PCR and sequencing. RESULTS: Of the 65 patients with benign parotid tumor, the frequencies of CC, CT, and TT genotypes were 33 (50.8%), 25 (38.5%), and 7 (10.7%), as compared to those of 44 (63.8%), 24 (34.8%), and 1 (1.4%) in the control group (P=0.05). The allele frequency of C/T was 70%/30% in patients with benign parotid tumor, significantly different from that in the control group (80.6%/19.4%, P<0.05). CONCLUSION: Rs6474051 polymorphism of PLAG1 gene may be associated with the benign parotid tumor in Chinese Han population in Hainan Province, and the T allele is probably one of susceptible genes.