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Merck

FAT1 inhibits cell migration and invasion by affecting cellular mechanical properties in esophageal squamous cell carcinoma.

Oncology reports (2018-03-23)
Xiaoling Hu, Yuanfang Zhai, Ruyi Shi, Yu Qian, Heyang Cui, Jie Yang, Yanghui Bi, Ting Yan, Jian Yang, Yanchun Ma, Ling Zhang, Yiqian Liu, Guodong Li, Mingsheng Zhang, Yongping Cui, Pengzhou Kong, Xiaolong Cheng
RESUMEN

FAT atypical cadherin 1 (FAT1) belongs to the cadherin superfamily and has been reported to regulate cell‑cell adhesion and other cell behaviors, suggesting its pivotal roles in human cancers. We previously identified FAT1 as one of the significant mutant genes in esophageal squamous cell carcinoma (ESCC). In the present study, the knockdown of FAT1 expression in YSE2 and Colo680N cell lines was carried out by lentivirus, and we found that knockdown of FAT1 led to acceleration of cell migration and invasion. Furthermore, we detected the cell adhesive force and cell elasticity force by atomic force microscopy (AFM) and found that the suppression of endogenous expression of FAT1 led to a decrease in the cell adhesive force and increase in the cell elasticity force compared with the control groups. In conclusion, our study demonstrated that FAT1 altered cellular mechanical properties leading to deregulation of cell migration and invasion of ESCC, which may be a novel target for ESCC therapy.

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Sigma-Aldrich
Anti-FAT1 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution