Activation Of TGF-β1/smad7 Signaling In ESCC Through Epithelial-Mesenchymal Transition

Objective: To investigate the effects and mechanism of TGF-β1/Smad7 signaling pathway in Kazakh’s esophageal squamous cell carcinoma(ESCC) through Epithelial-Mesenchymal Transition(EMT). Methods: Expression of TGF-β1 and Smad7 protein in carcinoma tissues and adjacent normal tissues of 72 Kazakh’s ESCC patients was detected by immunohistochemistry(IHC). Based on RNA interference technology, Ec9706 cell was transfected with TGF-β1 siRNA, using LipofectamineTM2000. The mRNA expression level of TGF-β1 and Smad7 were detected by qRT-PCR. Expression of TGF-β1, Smad7 and EMT-associated proteins were measured by Western blot after transfection. Then MTT, Wound-healing assay and Flow cytometry were performed to detect cell’s proliferation, migration, apoptosis and cell cycle after transfection. Results: The positive rate of TGF-β1 expression in carcinoma tissues of patients with ESCC was significantly higher than non-cancerous adjacent tissue(P﹤0.05), while the positive expression rates of Smad7 in ESCC tissues was significantly lower than the non-cancerous adjacent tissues(P ﹤ 0.05). TGF-β1 and Smad7 expression were negatively correlated(P<0.05, r =-0.253). After transfected with TGF-β1 siRNA, expression of TGF-β1 and Vimentin were significantly decreased, meanwhile, expression of Smad7 and E-cadherin were increased. Furthermore, transfected with TGF-β1 siRNA inhibited cell proliferation, migration and promoted cell apoptosis. Conclusion: TGF-β1/Smad7 signaling activates in Kazakh’s ESCC. TGF-β1 could promote EMT through inhibition of Smad7, consequently promote cell proliferation and migration, influence cell cycle at G0/G1 phase and inhibit the apoptosis of ESCC.