Lef1 enhances the progression of colonic adenocarcinoma via remodeling the cell motility associated structures
Xiao, L, Zhang, C, Li, X, Jia, C, Chen, L, Yuan, Y, Gao, Q, Lu, Z, Feng, Y, Zhao, R, Zhao, X, Cheng, S, Shu, Z, Xu, J, Duan, Wei, Nie, G and Hou, Y 2021, Lef1 enhances the progression of colonic adenocarcinoma via remodeling the cell motility associated structures, International Journal of Molecular Sciences, vol. 22, no. 19, pp. 1-14, doi: 10.3390/ijms221910870.
Attached Files
Name
Description
MIMEType
Size
Downloads
Title
Lef1 enhances the progression of colonic adenocarcinoma via remodeling the cell motility associated structures
Lymphoid enhancer-binding factor 1 (LEF1) is a key transcription factor mediating the Wnt signaling pathway. LEF1 is a regulator that is closely associated with tumor malignancy and is usually upregulated in cancers, including colonic adenocarcinoma. The underlying molecular mechanisms of LEF1 regulation for colonic adenocarcinoma progression remain unknown. To explore it, the LEF1 expression in caco2 cells was inhibited using an shRNA approach. The results showed that downregulation of LEF1 inhibited the malignancy and motility associated microstructures, such as polymerization of F-actin, β-tubulin, and Lamin B1 in caco2 cells. LEF1 inhibition suppressed the expression of epithelial/endothelial-mesenchymal transition (EMT) relevant genes. Overall, the current results demonstrated that LEF1 plays a pivotal role in maintaining the malignancy of colonic adenocarcinoma by remodeling motility correlated microstructures and suppressing the expression of EMT-relevant genes. Our study provided evidence of the roles LEF1 played in colonic adenocarcinoma progression, and suggest LEF1 as a potential target for colonic adenocarcinoma therapy
Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved.
Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO.
If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.
Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.