Abstract
The Wnt pathway alterations have been identified in colorectal and many other cancer types. It has been reported that galectin-3 (which is encoded by the LGALS3 gene) alters the signaling mechanism in the Wnt/β-catenin pathway by binding to β-catenin in colon and other cancers. AXIN1 is mainly responsible for the assembly of the β-catenin destruction complex in the Wnt pathway. This study investigated the relationship of rs4644 and rs4652 variants of the LGALS3 gene and rs214250 variants of the AXIN1 gene to histopathological and clinical properties. Our study included a total of 236 patients, of whom 119 had colorectal cancer (42 women, 77 men) and 117 were healthy controls. Polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) and allele-specific oligonucleotide (ASO) PCR methods were used. In addition, the serum galectin-3 level was studied with the enzyme-linked immunosorbent assay (ELISA) method. For the rs4644 variant of the LGALS3 gene, the CC genotype a mucinous component was significantly more common than those without a mucinous component (p=0.026). C allele frequency of the rs214250 variant of the AXIN1 gene was significantly correlated to tumor size in the advanced tumor stage (p=0.022). The CCAACT haplotype was more common in colorectal cancer patients (p=0.022). Serum galectin-3 level was higher in the patient group compared to the control group (5.9± 0.69 ng/ml vs. 0.79±0.01 ng/ml; p<0.001). In conclusion, variants of LGALS3 and AXIN1 genes affect tumor sizes and the mucinous component via Wnt/β-catenin pathway in the pathogenesis of colorectal cancer.
Highlights
Colorectal cancer (CRC) is the third most prevalent cancer in both sexes worldwide
No significant differences were found between the colorectal cancer and control groups with regard to genotype distribution and allelic frequencies for the rs214250 variant of the AXIN1 gene (p>0.05)
The AACC haplotype of the rs4652 variant of the LGALS3 gene and the rs214250 variant of the AXIN1 gene had a significantly lower frequency in the patient group compared to the control group (3.4% vs. 13.7%, p=0.004; OR: 0.246; 95%CI: 0.085-0.713)
Summary
Colorectal cancer (CRC) is the third most prevalent cancer in both sexes worldwide. It is the second most common cause of cancer-related mortality in both sexes [1]. It is responsible for 9.4% of newly diagnosed cancer cases in men and 10.1% in women [2]. About 70% of the CRC cases are sporadic, i.e. no familial or genetic contribution can be found [3]. Genetic alterations or genomic re-arrangements can lead to important changes in cells with respect. A thorough understanding of colorectal carcinogenesis requires the elucidation of genetic mechanisms responsible for tumor development
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