Relationship of SNP rs35767 in IGF-1 promoter region with susceptibility to colorectal cancer
In vitro and animal experiments demonstrate that IGF-1 appears to play a role in the development and growth of colorectal cancer and the function of free IGF-1 protein is mediated by IGF-1R. The IGF-1R system plays a critical role in promoting the normal development of cells and malignant transforma...
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Veröffentlicht in: | International journal of clinical and experimental pathology 2018-01, Vol.11 (10), p.5110-5116 |
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Sprache: | eng |
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Zusammenfassung: | In vitro and animal experiments demonstrate that IGF-1 appears to play a role in the development and growth of colorectal cancer and the function of free IGF-1 protein is mediated by IGF-1R. The IGF-1R system plays a critical role in promoting the normal development of cells and malignant transformation via the phosphatidylinositol 3-kinase (PI3)/AKTA and mitogen-activated protein kinase (MAPK) pathways. Different variants of the promoter of IGF-1 are involved in the risk of suffering from various diseases. The current study examined the relationship between IGF-1 rs35767 polymorphism and the risk of colorectal cancer (CRC) in a population from China. The genotypes of rs35767 polymorphism of the promoter region of IGF-1 were examined in 734 subjects: 367 patients with CRC and 367 healthy individuals by PCR. LDL and TC levels in colorectal cancer patients were significantly higher than those in the healthy control group (
). Compared with CC genotype carriers, people with the CT genotype had a 1.39-fold higher risk of CRC (
). There was no association between genotypes of rs35767 and the risk of CRC, after stratification according to gender. The patients who carried the T allele tend to have poor tissue differentiation. SNP rs35767 polymorphism associated with IGF-1 levels may be associated with susceptibility to colorectal cancer. People with the CT genotype may have a higher risk of CRC, and the patients who carried T allele tend to have poor tissue differentiation. |
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ISSN: | 1936-2625 |