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Updated: Jan 20, 2026
Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
Published on: October 9, 2014
TIS111D can affect bladder cancer cells by regulating epithelial-mesenchymal transition
Yin Lei1, Liu Yang1, Jing Hongwei1
1Urology Surgery, First Affiliated Hospital of China Medical University, Shenyang, PR China.
Aims:
Delineates the role of TIS111D in bladder cancer.
Materials And Methods:
The expression of TIS111D in bladder cancer and adjacent tissues was assessed by immunohistochemistry, Western blot and real-time PCR. Western blot and real-time PCR were used to analyse the expression of TIS111D in HT1197, T24, 5637 and TCCSUP cells. After TIS111D was silenced in T24, 5637 and TCCSUP cells, MTT and Transwell assays were used to detect the effects of TIS111D on proliferation and migration. Western blot and real-time PCR were used to detect the regulatory effect of downregulation of TIS111D on N-cad and E-cad. In vivo experiments confirmed the role of TIS111D in the growth and migration of bladder cancer and determined whether the role of TIS111D in bladder cancer is related to its regulation of N-cad and E-cad.
Key Findings:
The expression of TIS11D was higher in tumour tissues and bladder cancer cells. Si-TIS111D could inhibit the growth and migration of bladder cancer cells, while TIS111D could regulate the expression of E-cad and N-cad to regulate epithelial-mesenchymal transition (EMT). We also demonstrated that TIS111D could promote the growth and migration of bladder cancer in vivo by regulating EMT.
Significance:
TIS111D may participate in the regulation of bladder cancer progression by regulating EMT.
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