The Role And Molecular Mechanism Of Long Non-coding RNA SNHG16 In The Progression Of Cervical Cancer

Objective: This study revealed the role of LncRNA SNHG16 in the development of cervical cancer and its molecular mechanism through clinical data analysis,in vitro and in vivo experiments,and confirm that LncRNA SNHG16 is the key pathogenic molecule that mediates the malignant development of cervical cancer.Methods: To collect surgically resected cervical cancer tissues and normal cervical tissues;qRT-PCR to detect the expression levels of LncRNA SNHG16 in cervical cancer tissues,normal cervical tissues and cervical cancer cells;CCK8 assay and the clone formation experiment to detect the effect of LncRNA SNHG16 on the proliferation of cervical cancer cells;the scratch and Tanswell assay to detect the effect of LncRNA SNHG16 on the migration and invasion of cervical cancer cells;the Annexin V/7-AAD assay to detect the role of LncRNA SNHG16 silencing in apoptosis;the effect of LncRNA SNHG16 on the growth of cervical cancer tumors was detected in vivo;qRT-PCR to detect the expression level of PARP9 mRNA in normal and cervical cancer tissues,cervical cancer cells;the relationship between SNHG16 and PARP9 gene promoter activity was detected by the Dual luciferase reporter gene assay;RIP method was used to detect the binding of SNHG16 and SPI1 protein;ChIP method was used to detect the binding of SPI1 and PARP9 gene promoter;CCK8assay was used to detect the role of PARP9 in the proliferation of cervical cancer cells;Tanswell assay was used to detect the role of PARP9 in the invasion of cervical cancer cells.Western blotting detected the expression of PARP9,Ki67,PCNA,E-cadherin,Vimentin,MMP-2,MMP-9.Results: Compared with normal cervical tissue,the expression of LncRNA SNHG16 in cervical cancer tissue was significantly up-regulated(P < 0.05);compared with normal cervical epithelial cells Hcer Epic In contrast,the expression of LncRNA SNHG16 in cervical cancer cells Ca Ski,C33a,ME180,and HeLa was significantly up-regulated(P < 0.05);after silencing LncRNA SNHG16,the proliferation ability of C33a and HeLa cells was significantly weakened(P<0.05);after silencing LncRNA SNHG16,C33a The migration ability of cells was significantly weakened(P < 0.05),while the migration ability of HeLa cells was not affected;after silencing LncRNA SNHG16,the invasion ability of C33a and HeLa cells was significantly weakened;after silencing LncRNA SNHG16,the apoptosis level of C33a and HeLa cells In vivo experiments,silencing LncRNA SNHG16 can significantly inhibit tumor growth(P < 0.05);compared with Hcer Epic cells,the expression of PARP9 in HeLa cells was significantly increased(P < 0.05);LncRNA SNHG16 enhanced the activity of PARP9 gene promoter(P<0.05);LncRNA SNHG16 binds to the SPI1 protein;SPI1 binds to the PARP9 gene promoter;After LncRNA SNHG16 is silenced,the activity of the PARP9 gene promoter in Hela cells is significantly inhibited,and the PARP9 mRNA and protein expression levels are significantly reduced(P<0.05);after silencing LncRNA SNHG16,the proliferation and invasion ability of Hela cells was significantly weakened,but at the same time overexpression of PARP9 could restore its proliferation and invasion ability(P<0.05).Conclusion: 1)LncRNA SNHG16 is highly expressed in cervical cancer tissues and cervical cancer cells,and is significantly related to tumor diameter,degree of differentiation and tumor stage;2)Silencing LncRNA SNHG16 significantly inhibit the proliferation,migration and invasion of cervical cancer cells,promote the apoptosis of cervical cancer cells,and inhibit the growth of cervical cancer tumors;3)LncRNA SNHG16,as a pathogenic molecule,mediates the malignant proliferation and invasion of cervical cancer cells by activating the transcription of PARP9 gene regulated by SPI1,and ultimately promotes the malignant development of cervical cancer.