Upregulation of long noncoding RNA SNHG18 promotes radioresistance of glioma by repressing Sema5A

Publication date: Available online 30 July 2016
Source:International Journal of Radiation Oncology*Biology*Physics
Author(s): R. Zheng, Q.W. Yao, C. Ren, Y. Liu, H.L. Yang, G.Z. Xie, S.S. Du, K.J. Yang, Y.W. Yuan
Although there is increasing evidence that long noncoding RNAs (lncRNAs) play an important regulatory role in carcinogenesis and tumor progression, little is known about the role of small nucleolar RNA host gene 18 (SNHG18) in cancer. This study investigated the clinical associations of SNHG18 and its role in glioma. Our results showed that the expression level of SNHG18 was remarkably up-regulated in clinical glioma tissues compared with normal brain tissues.SNHG18 expression was associated with the clinical tumor grade and was negatively correlated with IDH1 mutation. In addition, knockdown of SNHG18 with short hairpin RNA suppressed the radioresistance of glioma cells, whereas transgenic expression of SNHG18 had the opposite effect. Furthermore, xenograft tumors grown from cells with SNHG18 deletion were more radiosensitive than tumors grown from control cells. Further studies revealed that SNHG18 promotes radioresistance by inhibiting Sema5A, and that inhibition of Sema5A expression abrogated the radiosensitizing effect caused by SNHG18 deletion. Our findings provide new insights into the role of SNHG18 in glioma, and suggest its potential as a target for glioma therapy.

Teaser

SNHG18 is significantly up-regulated in clinical glioma tissues and is negatively associated with Sema5A expression. Inhibition of SNHG18 is able to suppress glioma cell radioresistance. The promotion effect of SNHG18 deletion in radiosensitivity was rescued by suppression of Sema5A.


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