Aim of the study
This study explored the function of SNHG7 in CC and further investigates the specific molecular mechanism of SNHG7 in regulating CC.
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, SNHG7 has been reported to enhance the occurrence of various cancers; however, its function in CC sustains obscure.
Conclusions
SNHG7 epigenetically silences DKK1 to exacerbate the malignancy of CC via Wnt/β-catenin signaling pathway.
Methods
The levels of SNHG7 in CC cells were reflected by quantitative real-time polymerase chain reaction. The functions of SNHG7 on CC tumorigenesis were explored by colony formation, CCK-8 (Cell Counting Kit-8), EdU (ethynyl deoxyuridine), and Western blot assays. The influences of SNHG7 depletion on the binding of EZH2 to DKK1 promoter and H3K27me3 occupancy in DKK1 promoter were studied by chromatin immunoprecipitation assay.
Results
SNHG7 was conspicuously higher expressed in CC cells. Knockdown of SNHG7 was detected to ameliorate the malignant behaviors of CC cells. Importantly, the contribution of SNHG7 to CC development was relied on activated Wnt pathway through DDK1-mediated manner. Furthermore, it was confirmed that SNHG7 silencing weakened the binding of EZH2 to DKK1 promoter as well as the occupancy of H3K27me3 in DKK1 promoter. Conclusions: SNHG7 epigenetically silences DKK1 to exacerbate the malignancy of CC via Wnt/β-catenin signaling pathway.