Article Text
Abstract
Colorectal cancer (CRC) is the third most common cancer and one of the main causes of death around the world. Multiple lines of evidence have suggested the role of the corticotropin-releasing hormone (CRH) family in CRC induction, including the low expression of corticotropin-releasing hormone receptor 2 (CRHR2), which is an angiogenesis inhibitor and inflammatory modulator. Previous research suggests that CRHR2 expression in colonic intestinal cells can regulate migration, proliferation and apoptosis through the modulation of several pathways. The aim of this study was to analyze the association of the rs10250835, rs2267716 and rs2267717 variants of CRHR2 gene with CRC in the Mexican population in order to consider its predictive value in CRC. This cross-sectional study included a group of 187 unrelated patients with sporadic CRC and a control group of 191 healthy blood donors. DNA extraction from peripheral blood was carried out using the Miller method. Identification of the rs10250835 variant was performed using PCR-restriction fragment length polymorphism (RFLP) and the rs2267716 and rs2267717 variants using TaqMan allelic discrimination assay. The minor allele homozygous CC of the rs2267716 variant of CRHR2 showed significant difference between CRC and control group (p=0.025), as well as the GCA haplotype (p=0.007), corresponding to the rs10250835, rs2267716 and rs2267717 variants, respectively. Our results suggest that the rs2267716 variant and GCA haplotype of CRHR2 represent a risk factor for CRC development in Mexican patients.
- polymorphism
- restriction fragment length
- polymorphism
- genetic
- carcinogenesis
- colorectal neoplasms
Data availability statement
All data relevant to the study are included in the article or uploaded as supplementary information. All relevant data can be requested to the corresponding author to the mail nellymacias_2000@yahoo.com.mx.
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Data availability statement
All data relevant to the study are included in the article or uploaded as supplementary information. All relevant data can be requested to the corresponding author to the mail nellymacias_2000@yahoo.com.mx.
Footnotes
Contributors AAR-G, COG-V, EL-U, MG-A, MR-F, ID-E and NMM-G have contributed to design of the work and interpretation of data. Moreover, they have approved the final version. AAR-G, COG-V and NMM-G have worked with acquisition, analysis of molecular data and guarantor.
Funding The project was supported by Universidad de Guadalajara, México.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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