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Published on: February 5, 2018
CDH1 POLYMORPHISMS AND LOW EXPRESSION OF E-CADHERIN AND β-CATENIN IN COLORECTAL CANCER PATIENTS
M Martinelli1, A Palmieri1, M T Rodia1
1Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Bologna, Italy; Centre of Molecular Genetics, CARISBO Foundation, University of Bologna, Bologna, Italy.
Reduced expression of E-cadherin and β-catenin genes was observed in colorectal cancer tissues. These genes play a key role in the epithelial-mesenchymal transition (EMT) process, crucial for tumor progression.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Epithelial-mesenchymal transition (EMT) is critical for tumor progression and metastasis.
- Loss of cell adhesion, involving E-cadherin and β-catenin, is a key EMT step.
- Nuclear translocation of β-catenin activates transcription factors like LEF1, targeting EMT genes.
Purpose of the Study:
- To investigate the role of CDH1 (E-cadherin), CTNNB1 (β-catenin), and LEF1 genes in colorectal cancer (CRC).
- To assess the association between CDH1 polymorphisms and CRC in Italian patients.
- To analyze gene expression levels of CDH1, CTNNB1, and LEF1 in CRC tissues.
Main Methods:
- Association study of four CDH1 single nucleotide polymorphisms (SNPs) in 140 Italian CRC patients.
- Gene expression analysis of CDH1, CTNNB1, and LEF1 in 54 paired tumor and adjacent normal tissues from 27 CRC patients.
Main Results:
- No statistically significant association was found between the studied CDH1 polymorphisms and CRC.
- Reduced gene expression of CDH1 (E-cadherin) and CTNNB1 (β-catenin) was observed in cancer tissues compared to normal tissues.
- LEF1 gene expression levels were also analyzed in relation to CDH1 and CTNNB1 expression.
Conclusions:
- The study suggests reduced expression of E-cadherin and β-catenin in colorectal cancer tissues.
- A potential cross-regulation between CDH1 and CTNNB1 in EMT activation warrants further investigation in larger cohorts.
- The findings highlight the complex molecular mechanisms underlying EMT in colorectal cancer.
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