| Background/Aims: Bladder cancer,one of the most common urinary malignant cancers worldwide.The standard therapies for bladder cancer including surgery,radiotherapy,and chemotherapy are far from satisfactory.Therefore,it is necessary for us to develop a more efficient treatment for urinary bladder cancer.Enhancers are cis-acting elements that can promote the expression of target genes.It has been reported that enhancers respond to estrogen to induce the transcription of eRNAs,and these estrogen-related eRNAs are closely associated with the molecular mechanisms of estrogen in breast cancer.Further study on eRNAs may lead to a better understanding of the progression of malignant tumors and the significance of transcriptional regulation.SMAD7 enhancer RNA(SMAD7e)is an estrogen-responsive eRNA.However,the relationship between SMAD7 e and bladder cancer remains unclear.Methods: The relative expression level of SMAD7 e was determined by real-time qPCR.We utilized CRISPR-Cas13 a to measure the effect of SMAD7 e knockdown on biological behaviors of bladder cancer cells.We used both CCK-8 and Edu assays to detect cell proliferation.Cell migration was detected by wound healing assays.Cell apoptosis was determined by ELISA assays.Cell invasion was detected by Transwell? assays.Results: SMAD7 e was significantly upregulated in bladder cancer tissues and estrogen-stimulated cells.Knockdown of SMAD7 e suppressed cell proliferation and migration,and induced cell apoptosis and repressed cell invasion.Estrogen caused overexpression of SMAD7 e and played a facilitating role in bladder cancer cells.Furthermore,knockdown of SMAD7 e prevented the cancer-promoting effects of estrogen on bladder cancer.Conclusion: The present study suggested the crucial role of SMAD7 e in bladder cancer.Estrogen might promote the development of bladder cancer by inducing SMAD7 e production.These findings may provide a potential target for diagnosis and gene therapy for bladder cancer in the future. |
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