Purpose: A long noncoding RNA called small nucleolar RNA host gene 7 (SNHG7 ) is known to be a key regulator of biological processes in multiple human cancer types. In this study, our aims were to determine the expression status of SNHG7  in cervical cancer, to figure out the detailed roles of SNHG7  in cervical cancer cells, and to identify the mechanism underlying the activity of SNHG7  in cervical cancer.
Methods: Reverse-transcription quantitative PCR was performed to measure SNHG7  expression in cervical cancer. A Cell Counting Kit-8 assay, flow-cytometric analysis, cell migration and invasion assays, and a tumor xenograft experiment were conducted to respectively determine the effects of SNHG7  on cervical cancer cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo.
Results: SNHG7  was found to be markedly upregulated in cervical cancer tissues and cell lines. Higher SNHG7  expression significantly correlated with FIGO stage, lymph node metastasis, the depth of cervical invasion, and shorter overall survival in patients with cervical cancer. Functional experiments indicated that a SNHG7  knockdown attenuated proliferation, migration, and invasiveness and promoted apoptosis of cervical cancer cells in vitro. The SNHG7  knockdown also slowed tumor growth in vivo. Further investigation showed that SNHG7  acts as a competing endogenous RNA for microRNA-485 (miR-485) in cervical cancer cells, and the inhibitory actions of the SNHG7  knockdown on the malignant phenotype were reversed by miR-485 inhibition. P21-activated kinase 4 (PAK4 ) was identified as a direct target gene of miR-485 in cervical cancer, and PAK4 expression was promoted by SNHG7 .
Conclusion: SNHG7  functions as an oncogenic RNA in cervical cancer, competitively binds to miR-485, and thereby upregulates PAK4. This SNHG7 –miR-485–PAK4 regulatory network may provide insights into the pathogenesis of cervical cancer, and can help in the identification of novel diagnostic and therapeutic approaches for cervical cancer.
Keywords: small nucleolar RNA host gene 7, P21-activated kinase 4