Delta-catenin promotes the proliferation and invasion of colorectal cancer cells by binding to E-cadherin in a competitive manner with p120 catenin

2013 ◽  
Vol 9 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Hong Zhang ◽  
Shun-Dong Dai ◽  
Di Zhang ◽  
Dong Liu ◽  
Fang-Yuan Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
P120 Catenin ◽  
Colorectal Cancer Cells ◽  
Proliferation And Invasion ◽  
E Cadherin

scholarly journals APC regulation of ESRP1 and p120-catenin isoforms in colorectal cancer cells

2020 ◽  
pp. mbc.E20-05-0321
Author(s):  
Maree C. Faux ◽  
Lauren E. King ◽  
Serena R. Kane ◽  
Christopher Love ◽  
Oliver M. Sieber ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Adhesion ◽  
Wnt Signaling ◽  
Cancer Cells ◽  
Full Length ◽  
P120 Catenin ◽  
Colorectal Cancer Cells ◽  
Isoform Switching ◽  
E Cadherin ◽  
Cell Cell

The APC tumor suppressor protein is associated with the regulation of Wnt signaling, however APC also controls other cellular processes including the regulation of cell adhesion and migration. The expression of full-length APC in SW480 colorectal cancer cells (SW480+APC) not only reduces Wnt signaling, but increases membrane E-cadherin and restores cell-cell adhesion. This report describes the effects of full-length, wild-type APC (fl-APC) on cell-cell adhesion genes and p120-catenin isoform switching in SW480 colon cancer cells: fl-APC increased the expression of genes implicated in cell-cell adhesion, whereas the expression of negative regulators of E-cadherin were decreased. Analysis of cell-cell adhesion-related proteins in SW480+APC cells revealed an increase in p120-catenin isoform 3A; similarly, depletion of APC altered the p120-catenin protein isoform profile. Expression of ESRP1 (epithelial splice regulatory protein 1) is increased in SW480+APC cells and its depletion results in reversion to the p120-catenin isoform 1A phenotype and reduced cell-cell adhesion. ESRP1 transcript is reduced in primary CRC and its expression correlates with the level of APC. Pyrvinium pamoate, which inhibits Wnt signaling, promotes ESRP1 expression. We conclude that re-expression of APC restores cell-cell adhesion gene and post-transcriptional regulatory programs leading to p120-catenin isoform switching and associated changes in cell-cell adhesion.

scholarly journals MK615 Suppresses Hypoxia Tolerance by Up-regulation of E-cadherin in Colorectal Cancer Cells With Mutant KRAS

2020 ◽  
Vol 40 (8) ◽  
pp. 4687-4694
Author(s):  
KENSUKE NISHI ◽  
TOSHIYUKI TSUNODA ◽  
YOSHINORI UCHIDA ◽  
TAKAYUKI SUETA ◽  
MOTOHIRO SAWATSUBASHI ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Hypoxia Tolerance ◽  
Colorectal Cancer Cells ◽  
E Cadherin

Loss of E-cadherin promotes the growth, invasion and drug resistance of colorectal cancer cells and is associated with liver metastasis

2012 ◽  
Vol 39 (6) ◽  
pp. 6707-6714 ◽  
Author(s):  
Xiaobing Chen ◽  
Yongsheng Wang ◽  
Hongping Xia ◽  
Qiwu Wang ◽  
Xiaochun Jiang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistance ◽  
Liver Metastasis ◽  
Cancer Cells ◽  
Colorectal Cancer Cells ◽  
E Cadherin

scholarly journals Correlation between FAK and EGF-Induced EMT in Colorectal Cancer Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Kun Huang ◽  
Ningning Gao ◽  
Donglin Bian ◽  
Qixi Zhai ◽  
Puxu Yang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Egfr Signaling Pathway ◽  
Colorectal Cancer Cells ◽  
E Cadherin

Epithelial-mesenchymal transition (EMT) plays an important role in the invasion and metastasis of colorectal cancer, which is mediated by FAK and EGF. However, whether FAK participates in EMT in colorectal cancer cells through the EGF/EGFR signaling pathway remains unknown. The aim of this study was to investigate the effector mechanisms of FAK in the process of EGF-induced EMT in colorectal cancer cells and to determine whether miR-217 is involved in this process. Caco-2 cancer cells were routinely cultured with and without treatment with 100 ng/mL EGF, and changes in cell morphology were observed using an inverted microscope. In addition, a transwell assay was used to detect cell migration under the condition of EGF treatment. The expression of FAK, pFAK, E-cadherin, vimentin, and β actin was assessed by western blotting, and the expression of miR-217 was assessed using real-time PCR. We found that EGF induced EMT in colorectal cancer cells and enhanced cell migration and invasion ability. Moreover, FAK was involved in the EGF-induced EMT of colorectal cancer cells. EGF upregulated the expression of E-cadherin in colorectal cancer cells by activating FAK, and miR-217 was found to participate in EGF-induced EMT in colorectal cancer cells. Our findings indicate that EGF induces EMT in colorectal cancer cells by activating FAK, and miR-217 is involved in the EGF/FAK/E-cadherin signaling pathway.

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