| ObjectiveBladder cancer is the most common urothelial tumor.Muscle infiltration or distant metastasis of cancer cells will seriously affect the prognosis and quality of life of patients with bladder cancer.Emerging viewpoints suggest that the invasion and metastasis of bladder cancer cells belong to the epithelial-mesenchymal transition(EMT)process of cancer cells.During the development of bladder cancer disease,non-invasive bladder cancer transfers to invasive bladder is a process of reverse differentiation.How to control and inhibit the development of bladder cancer disease will help the prognosis of bladder cancer patients.But the mechanism of EMT in bladder cancer is unclear.In this paper,through the analysis of transcription factor regulatory pathways,to find out the mechanisms that potentially affect the reverse differentiation of bladder cancer.MethodsThe mechanism of reverse differentiation of bladder cancer cells was found out by analyzing the regulatory pathways of transcription factors.Then,cell function studies confirmed that transcription factor YY1 has a cell fate-determining effect on bladder cancer.The biological pathway TGFβ affecting the fate of bladder cancer cells was analyzed by transcriptome sequencing,and then verified.ResultsThe transcription factor YY1 expression in invasive bladder cancer is higher than normal bladder mucosa.Transcription factor YY1 interference and overexpression in bladder mucosal epithelial cancer cells.EMT ability of bladder cancer cells changed in YY1 expression group.It was determined that transcription factor YY1 was positively correlated with the promotion of EMT in bladder cancer cell.YY1 can affect the fate decision of bladder cancer through TGFβ pathway.ConclusionInterfering with YY1 expression indirectly reduces the EMT potential of bladder cancer cells by affecting the TGFβ pathway,which is also the mechanism that determines the fate of bladder cancer cells.The study of the transcription factor YY1 reveals the biological mechanism of bladder tumorigenesis and malignant progression,and provides a potential biological marker and therapeutic target.Figure 7 table 1 reference 32... |
