TSPAN7 promotes the migration and proliferation of lung cancer cells via epithelial-to-mesenchymal transition
Authors Wang X, Lin M, Zhao J, Zhu S, Xu M, Zhou X
Received 12 March 2018
Accepted for publication 8 August 2018
Published 13 December 2018 Volume 2018:11 Pages 8815—8822
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Takuya Aoki
Xianguo Wang,1,* Min Lin,2,* Jinping Zhao,1 Shaoping Zhu,1 Ming Xu,1 Xuefeng Zhou1
1Thoracic and Cardiovascular Surgery, Zhongnan Hospital of Wuhan University, Wuchang District, Wuhan, Hubei 430071, China; 2Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China
*These authors contributed equally to this work
Purpose: To explore the effects and mechanisms of tetraspanin TSPAN7 on the progression of non-small-cell lung cancer (NSCLC) cells.
Patients and methods: All 125 lung cancer specimens and 60 metastatic tissues were obtained from patients diagnosed with NSCLC, and we used immunohistochemistry to detect the expression of TSPAN7 in NSCLC tissues and adjacent normal tissues. Cell proliferation and invasion ability were determined by MTT, colony formation, and cell migration. The relative protein expression level was analyzed by Western blot analysis.
Results: Our clinical data showed that among 125 patients with lung cancer, TSPAN7 was associated with lymph node status, differentiation, tumor size, and poor prognosis. TSPAN7 knockout inhibited cell proliferation and migration. In addition, TSPAN7 increased the expression of N-cadherin in NSCLC cells by reducing the expression of E-cadherin and vimentin and promoting the cell epithelial–mesenchymal transition (EMT) process. Xenograft transplantation model confirmed the role of TSPAN7 in NSCLC metastasis.
Conclusion: TSPAN7-mediated EMT is the key to NSCLC migration. TSPAN7 is a potential target for NSCLC therapy.
Keywords: TSPAN7, non-small-cell lung cancer, cell invasion, colony formation
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