E-cadherin protein expression is significantly reduced in sporadic colorectal cancers (CRC), but apparently not as a consequence of allele loss or somatic mutation.
A conclusion could be drawn from the research that CDH1 -C160A polymorphism provides a possible protection against CRC, which is especially evident in Caucasian and hospital populations.
A further subgroup analysis by type of control tissues suggested that CRC tissues also exhibited higher frequencies of CDH1 promoter methylation than those of normal and adjacent tissues (normal: OR=1.57, 95% CI=1.12-2.21, p=0.009; adjacent: OR=5.07, 95% CI=2.91-8.82, p<0.001; respectively).
Absent or decreased E-cadherin protein expression was found in 27 (38%) of 68 colorectal cancers and the pattern of expression did not differ significantly among the three tumour groups.
Consolidated results of the fluorescency of all of the differential genes, designated two coding E-cadherin (CDH1) with the lower expression, and P-cadherin (CDH3) with higher expression in CRC tissue.
Following GWAS and candidate studies evaluated the association between the CDH1rs9929218 polymorphism and CRC in European, Asian and American populations.
For this reason, methylation of the CDH1 promoter is an attractive new biomarker for detecting ulcerative colitis patients with a high risk for developing colorectal cancers.
Genome-wide association studies (GWAS) in colorectal cancer (CRC) identified five regions near transforming growth factor β-related genes BMP4, GREM1, CDH1, SMAD7 and RPHN2.
Here, we examine CpG island methylation of 10 genes (hMLH1, BRCA1, APC, LKB1, CDH1, p16(INK4a), p14(ARF), MGMT, GSTP1 and RARbeta2) and 5-methylcytosine DNA content, in inherited (n = 342) and non-inherited (n = 215) breast and colorectal cancers.
In a population-based case-control study (498 cases and 600 controls), we assessed the association of CCND1 G870A and CDH1C-160A polymorphisms with CRC risk.
In addition, to better understand the role of CCND1 and CDH1 in the pathophysiology of CRC, the expression pattern was evaluated in analogous tumor and adjacent normal tissues from 23 CRC patients by Western blot analysis.
In conclusion, heterozygosity and mutant homozygosity as well as the combination of both TP53 Arg72Pro and CDH1rs16260 polymorphisms are responsible to increase the risk of colorectal cancer development in Bangladeshi population.
In immunofluorescence analysis, CLY exhibited a low expression but high restricted nuclear localization of beta-catenin and a silenced expression of E-cadherin, which may be induced by hypermethylation of the E-cadherin gene (CDH1) promoter and differed from conventional CRC cell lines.