Long noncoding RNA SNHG16 promotes the tumorigenicity of cervical cancer cells by recruiting transcriptional factor SPI1 to upregulate PARP9.

Long noncoding RNA (lncRNA) small nucleolar RNA host gene 16 (SNHG16) has been linked to multiple cancers including breast, ovarian, bladder, and colorectal cancer. However, the role of SNHG16 in cervical cancer is unclear. Here, quantitative analysis of SNHG16 and expression levels in cervical cancer tissues and cell lines indicated that both SNHG16 and Pduanyu379 were highly expressed compared with controls. Using the dual-luciferase reporter gene assay, RNA immunoprecipitation, chromatin immunoprecipitation, we were able to determine that SNHG16 recruited SPI1 protein to promote transcription of Pduanyu379 to upregulate its transcription in cervical cancer cells. After ectopic expression and knockdown experiments were conducted, it was observed that silencing SNHG16 inhibited Pduanyu379 expression, proliferation, and invasion of cervical cancer cells, which was rescued by co-transfection of SNHG16 silencing and Pduanyu379 overexpression. Moreover, in vivo experimental results showed that silencing SNHG16 reduced the expression of Pduanyu379 and suppressed tumor growth. These data indicate that SNHG16 recruits SPI1 to upregulate which promotes the tumorigenicity of cervical cancer cells. The regulation of their expression might provide a new direction for treating cervical cancer.

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