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Upregulation of T-cadherin suppresses cell proliferation, migration and invasion of gastric cancer in vitro.

Abstract
As a unique member of the cadherin superfamily, T-cadherin (T-cad) has been demonstrated to be associated with gastric cancer (GC) prognosis. To elucidate the function of T-cad in GC in vitro, the present study firstly examined T-cad protein expression in normal and gastric cancer tissues and cell lines, and it was demonstrated to be significantly downregulated in gastric cancer samples compared with normal samples. Control and T-cad expression vectors were then transfected into the MGC8-03 and AGS GC cell lines. Utilizing MTT, clonogenic, flow cytometry, wound healing and Transwell invasion assays in addition to Western blotting, the present study demonstrated that the overexpression of T-cad suppressed GC cell growth and colony formation via cell cycle arrest at the G0/G1 phase via downregulating the expression of cyclin dependent kinase 4 and Cyclin D1. In addition, overexpression of T-cad significantly inhibited GC cell migration and invasion by increasing E-cadherin and decreasing Vimentin expression. These findings suggest T-cad may be important in GC cell proliferation and metastasis and serve as a promising target for the treatment of GC in the future.
AuthorsJianqing Lin, Zhiyao Chen, Zhijun Huang, Feng Chen, Zeyi Ye, Shaoze Lin, Weidong Wang
JournalExperimental and therapeutic medicine (Exp Ther Med) Vol. 14 Issue 5 Pg. 4194-4200 (Nov 2017) ISSN: 1792-0981 [Print] Greece
PMID29104635 (Publication Type: Journal Article)

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