•  Home
  • Library
  • DRO home
Submit research Contact DRO

DRO

Openly accessible

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
Author(s) 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, WeiORCID iD for Duan, Wei orcid.org/0000-0001-5782-9184
Nie, G
Hou, Y
Journal name International Journal of Molecular Sciences
Volume number 22
Issue number 19
Article ID 10870
Start page 1
End page 14
Total pages 14
Publisher MDPI
Place of publication Basel, Switzerland
Publication date 2021-10
ISSN 1661-6596
1422-0067
Keyword(s) Biochemistry & Molecular Biology
CANCER
cancer malignancy
CATENIN
cell microstructures
Chemistry
Chemistry, Multidisciplinary
colonic cancer
CYTOSKELETON
EMT
EXPRESSION
INVASION
LEF1
Life Sciences & Biomedicine
MIGRATION
NOTCH
Physical Sciences
Science & Technology
Summary 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
Language eng
DOI 10.3390/ijms221910870
Field of Research 0399 Other Chemical Sciences
0604 Genetics
0699 Other Biological Sciences
HERDC Research category C1 Refereed article in a scholarly journal
Free to Read? Yes
Persistent URL http://hdl.handle.net/10536/DRO/DU:30157043

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
Open Access Collection
Related Links
Link Description
Link to full-text (open access)  
Connect to Elements publication management system
Go to link with your DU access privileges
 
Connect to link resolver
 
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.

Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 0 times in TR Web of Science
Scopus Citation Count Cited 0 times in Scopus Google Scholar Search Google Scholar
Access Statistics: 47 Abstract Views, 1 File Downloads  -  Detailed Statistics
Created: Fri, 15 Oct 2021, 08:00:35 EST

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.