Long Noncoding RNASNHG7Activates Wnt/beta-Catenin Signaling Pathway in Cervical Cancer Cells by Epigenetically SilencingDKK1

摘要

Background:Cervical cancer (CC) ranks fourth in cancers that resulted in death among women, accumulating the attention of researchers. It has been ascertained that long noncoding RNAs (lncRNAs) are crucial players in the pathological processes of a host of cancers. And,SNHG7has been reported to enhance the occurrence of various cancers; however, its function in CC sustains obscure. Aim of the Study:This study explored the function ofSNHG7in CC and further investigates the specific molecular mechanism ofSNHG7in regulating CC. Methods:The levels ofSNHG7in CC cells were reflected by quantitative real-time polymerase chain reaction. The functions ofSNHG7on CC tumorigenesis were explored by colony formation, CCK-8 (Cell Counting Kit-8), EdU (ethynyl deoxyuridine), and Western blot assays. The influences ofSNHG7depletion on the binding ofEZH2toDKK1promoter andH3K27me3occupancy inDKK1promoter were studied by chromatin immunoprecipitation assay. Results:SNHG7was conspicuously higher expressed in CC cells. Knockdown ofSNHG7was detected to ameliorate the malignant behaviors of CC cells. Importantly, the contribution ofSNHG7to CC development was relied on activated Wnt pathway through DDK1-mediated manner. Furthermore, it was confirmed thatSNHG7silencing weakened the binding ofEZH2toDKK1promoter as well as the occupancy ofH3K27me3inDKK1promoter. Conclusions:SNHG7epigenetically silencesDKK1to exacerbate the malignancy of CC via Wnt/beta-catenin signaling pathway.