Dataset Information

The Role of PPAR-gamma C161T Polymorphism in Colorectal Cancer Susceptibility.

ABSTRACT:

Background/aim

This study aimed to determine the role of the peroxisome proliferator-activated receptor-gamma (PPARg) C161T genotype and allele frequencies in predisposition to colorectal cancer (CRC).

Patients and methods

PPARg C161T (His447His; rs3856806) gene polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism analysis in patients with CRC (n=101) and controls (n=238).

Results

The T161 allele (CT+TT genotypes) of PPARg C161T polymorphism was associated with CRC development (p<0.001; OR=3.239, 95%CI=1.997-5.252). Subgroup analysis showed that the T161 allele was associated with a 3.056-fold increased risk for colon cancer (CC) (p<0.001; 95%CI=1.709-5.464) and 3.529-fold increased risk for rectal cancer (RC) (p<0.001; 95%C=1.784-6.981). Frequencies of the T161 allele were also higher in total CRC and CC patients with poorly differentiated tumors (p<0.001, c²=30,601, OR=3.109; 95%CI=1.970-4.906 and p<0.001, Fisher exact test, respectively).

Conclusion

PPARg T161 allele carriers have increased risk for developing CRC.

SUBMITTER: Kurnaz-Gomleksiz O

PROVIDER: S-EPMC9301400 | biostudies-literature | 2022 Jul-Aug

REPOSITORIES: biostudies-literature

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Publications

The Role of PPAR-gamma C161T Polymorphism in Colorectal Cancer Susceptibility.

Kurnaz-Gomleksiz Ozlem O Torun Bahar Canbay BC Isbir Turgay T Bulut Turker T Sokucu Necmettin N Yilmaz-Aydogan Hulya H Canbay Emel E

In vivo (Athens, Greece) 20220701 4

<h4>Background/aim</h4>This study aimed to determine the role of the peroxisome proliferator-activated receptor-gamma (PPARg) C161T genotype and allele frequencies in predisposition to colorectal cancer (CRC).<h4>Patients and methods</h4>PPARg C161T (His447His; rs3856806) gene polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism analysis in patients with CRC (n=101) and controls (n=238).<h4>Results</h4>The T161 allele (CT+TT genotypes) of PPARg C161 ...[more]

PMID: 35738614

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Project description:BackgroundIntestinal fibrosis is characterized by abnormal production and deposition of extracellular matrix (ECM) proteins by activated myofibroblasts. The main progenitor cells of activated myofibroblasts are the fibroblasts and the epithelial cells, the latter through the epithelial-mesenchymal transition (EMT).AimTo evaluate the action of the new PPAR-γ modulator, GED-0507-34 Levo (GED) on the expression of EMT associated and regulatory proteins such as TGF-β, Smad3, E-cadherin, Snail, ZEB1, β-catenin, and GSK-3β, in a mouse model of DSS-induced intestinal fibrosis.MethodsChronic colitis and fibrosis were induced by oral administration of 2.5% DSS (w/v) for 6 weeks. GW9662 (GW), a selective PPAR-γ inhibitor, was also administered by intraperitoneal injection at the dose of 1 mg/kg/day combined with GED treatment. All drugs were administered at the beginning of the second cycle of DSS (day 12). 65 mice were randomly divided into five groups (H2O as controls n = 10, H2O+GED n = 10, DSS n = 15, DSS+GED n = 15, DSS+GED+GW n = 15). The colon was excised for macroscopic examination and histological and morphometric analyses. The level of expression of molecules involved in EMT and fibrosis, like TGF-β, Smad3, E-cadherin, Snail, ZEB1, β-catenin, GSK-3β and PPAR-γ, was assessed by immunohistochemistry, immunofluorescence, western blot and Real Time PCR.ResultsGED improved the DSS-induced chronic colitis and fibrosis. GED was able to reduce the expression of the main fibrosis markers (α-SMA, collagen I-III and fibronectin) as well as the pivotal pro-fibrotic molecules IL-13, TGF-β and Smad3, while it increased the anti-fibrotic PPAR-γ. All these GED effects were nullified by co-administration of GW with GED. Furthermore, GED was able to normalize the expression levels of E-cadherin and β-catenin and upregulated GSK-3β, that are all known to be involved both in EMT and fibrosis.ConclusionsThe DSS-induced intestinal fibrosis was improved by the new PPAR-γ modulator GED-0507-34 Levo through the modulation of EMT mediators and pro-fibrotic molecules and through GSK-3β induction.

Dataset Information

The Role of PPAR-gamma C161T Polymorphism in Colorectal Cancer Susceptibility.

Background/aim

Patients and methods

Results

Conclusion

Publications

The Role of PPAR-gamma C161T Polymorphism in Colorectal Cancer Susceptibility.

Similar Datasets

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