Long non-coding RNA SNHG20 promotes nasopharyngeal carcinoma cell migration and invasion by upregulating TGF-β1.

Small nucleolar RNA host gene 20 (SNHG20) has been reported to serve roles in several types of malignancies, while its role in nasopharyngeal carcinoma remains unknown. In the present study, tumor tissues and adjacent healthy tissues of patient with nasopharyngeal carcinoma, as well as blood samples from patients with nasopharyngeal carcinoma and heathy controls were collected, and expression levels of SNHG20 were detected by reverse transcription-quantitative polymerase chain reaction. Receiver operating characteristic curve and survival curve analyses were performed to evaluate the diagnostic and prognostic values of SNHG20 expression for nasopharyngeal carcinoma, respectively. Associations between serum expression levels of SNHG20 and clinical data of patients with nasopharyngeal carcinoma were analyzed using χ2 test. A SNHG20 expression vector was constructed and transfected into nasopharyngeal carcinoma cells, and cell migration and invasion were detected by Transwell assays. Expression of transforming growth factor-β1 (TGF-β1) was detected by western blotting. Results indicated that the expression level of SNHG20 increased in cancer tissues compared with healthy tissues of patients with nasopharyngeal carcinoma. Serum level of SNHG20 increased in patients with nasopharyngeal carcinoma compared with healthy controls. Significant association was identified between serum levels of SNHG20 and distant tumor metastasis. Serum SNHG20 could serve as a potential diagnostic and prognostic marker for nasopharyngeal carcinoma. Overexpression of SNHG20 promoted nasopharyngeal carcinoma cell migration and invasion, and promoted the expression of TGF-β1. TGF-β1 inhibitor reduced the effects of SNHG20 overexpression on nasopharyngeal carcinoma cell migration and invasion, and exhibited no significant effect on SNHG20 expression. Therefore, the results of the present study indicated that lncRNA SNHG20 could promote the migration and invasion of nasopharyngeal carcinoma cells by upregulating TGF-β1.