Peroxisome Proliferator-Activated Receptor Gamma Pro12Ala/C161T Genotypes and Risky Haplotype Altering Risk of Breast Cancer: A Turkish Case–Control Study

Unal, Ersin Selcuk; Aslan, Ezgi; Öztürk, Tülin; Gömleksiz, Özlem Kurnaz; Küçükhüseyin, Özlem; Tuzuner, Mete Bora; Seyhan, Mehmet Fatih; Öztürk, Oğuz; Yilmaz-Aydogan, Hülya

doi:10.1007/s10528-021-10068-5

Cited by 3 publications

(2 citation statements)

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“…In a study, the heterozygous CT genotype of rs3856806 was found to be protective against colorectal cancer, however, in contrast, studies by Jiang et al and Lin et al showed an increased risk of colorectal cancer with this genotype [ 31 , 56 , 57 ]. Similarly, several studies have been conducted on breast cancer susceptibility, but the results remain debated [ 38 , 58 , 59 ] . Recently, two meta-analyses reported that the PPARγ rs3856806 C > T variant increased overall cancer susceptibility [ 60 , 61 ].…”

Section: Discussionmentioning

confidence: 99%

“…The rs1801282 SNV has been reported to be associated with susceptibility to a variety of tumors. However, in some studies such as on breast and colorectal cancers, the correlation tended to vary by race and/or cancer type [34,[36][37][38][39][40][41][42]. Several studies focused on the association of rs1801282 SNV with the susceptibility of GC.…”

Section: Discussionmentioning

confidence: 99%

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Association between PPARγ, PPARGC1A, and PPARGC1B genetic variants and susceptibility of gastric cancer in an Eastern Chinese population

Chen

Wang²,

Tang

et al. 2022

BMC Med Genomics

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Purpose Previous studies showed that peroxisome proliferator-activated receptor gamma (PPARγ) and PPARγ coactivator1 family (PPARGC1A and PPARGC1B) gene single nucleotide variants (SNVs)were strongly associated with cancer susceptibility. The purpose of this study was to investigate the association of PPARγ, PPARGC1A, and PPARGC1B variants with the risk of gastric cancer (GC). Patients and methods We performed a case-control study of 490 GC cases and 1,476 healthy controls from eastern China. PPARγ rs1801282 C > G, rs3856806 C > T, PPARGC1A rs2970847 C > T, rs8192678 C > T and PPARGC1B rs7732671 G > C, rs17572019 G > A SNVs were selected to investigate the association between these SNVs and GC susceptibility. Genotypes of the SNVs were assessed by multiplex fluorescent PCR using a custom-by-design 48-Plex SNPscantm Kit. Results The PPARγ rs1801282 SNV was associated with a decreased risk for GC (GC vs. CC: odds ratio (OR) = 0.62, 95% confidence interval (95%CI) = 0.42–0.93, adjusted P = 0.019; GC + GG vs. GG: OR = 0.63 95%CI = 0.42–0.93, adjusted P = 0.019; respectively). In addition, stratified analysis revealed that the PPARγ rs1801282 SNV was correlated with the risk of GC in subgroups of age ≥ 61, no smoking, and no alcohol consuming. We also confirmed that the PPARγ rs3856806 C > T SNV promoted the risk of GC in women. The PPARGC1A rs8192678 TT genotype decreased the susceptibility of GC in men. The PPARGC1A rs2970847 C > T SNV decreased the susceptibility of GC in the subgroup of BMI ≥ 24 kg/m2. The PPARGC1B rs7732671 G > C and rs17572019 G > A SNVs promoted the risk of GC in the subgroup of BMI ≥ 24 kg/m2. Conclusion This study indicates that the PPARγ, PPARGC1A, and PPARGC1B SNVs may be associated with the susceptibility of GC in eastern Chinese population. Future studies with larger populations, detailed H. pylori infection status for subgroup analysis, and functional study are needed to further clarify the relationship between these SNVs and GC risk.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Association between PPARγ, PPARGC1A, and PPARGC1B genetic variants and susceptibility of gastric cancer in an Eastern Chinese population

Chen

Wang²,

Tang

et al. 2022

BMC Med Genomics

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Joint effects of PPARG-C161T (rs3856806) polymorphism and cardiovascular risk factors on restenosis risk after coronary stent implantation

Javadova,

Yanar,

Aslan

et al. 2024

Turkish Journal of Biochemistry

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Objectives The peroxisome proliferator-activated receptor gamma (PPARG) C161T polymorphism (rs3856806) may be a risk factor for in-stent restenosis (ISR) due to its known associations with type 2 diabetes (T2DM), obesity, and coronary artery disease (CAD). This study aims to investigate the relationship between PPARG-C161T polymorphism and the risk of ISR, considering clinical features. Methods According to the results of coronary angiography, the patients who had undergone drug-eluting stent implantation were categorized into two groups: ISR (n=116) and non-ISR (n=265). The control group consisted of 140 healthy subjects with asymptomatic for CAD or any systemic disease. PPARG-C161T genotypes were determined using the real-time polymerase chain reaction melting curve analysis. Results T2DM, hypertension, and hyperlipidemia were observed as the main clinical features causing non-ISR and ISR. The 161-CC genotype was associated with an increased risk of ISR compared to both controls (p=0.014) and non-ISR patients (p=0.008). This difference remained statistically significant after multivariate analysis for non-ISR patients (p=0.003) but not for the ISR group. The prevalence of hypertension and hyperlipidemia was higher in ISR patients with T2DM than in non-ISR patients with T2DM (p=0.002 and p=0.009, respectively). Multivariate logistic regression analysis in subgroups based on the presence of T2DM showed that hypertension (p<0.001) was associated with ISR in patients with T2DM. Conclusions This study points out the association between the PPARG 161-CC genotype and the risk of ISR, which also means that the PPARG 161-T allele is protective against ISR. However, this effect could be divergent in the presence of the metabolic components of the restenosis phenotype, especially T2DM.

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PPARs and Tumor Microenvironment: The Emerging Roles of the Metabolic Master Regulators in Tumor Stromal–Epithelial Crosstalk and Carcinogenesis

Cheng

Yip

Lim

et al. 2021

Cancers

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Peroxisome proliferator-activated receptors (PPARs) have been extensively studied for more than three decades. Consisting of three isotypes, PPARα, γ, and β/δ, these nuclear receptors are regarded as the master metabolic regulators which govern many aspects of the body energy homeostasis and cell fate. Their roles in malignancy are also increasingly recognized. With the growing interest in crosstalk between tumor stroma and epithelium, this review aims to highlight the current knowledge on the implications of PPARs in the tumor microenvironment. PPARγ plays a crucial role in the metabolic reprogramming of cancer-associated fibroblasts and adipocytes, coercing the two stromal cells to become substrate donors for cancer growth. Fibroblast PPARβ/δ can modify the risk of tumor initiation and cancer susceptibility. In endothelial cells, PPARβ/δ and PPARα are pro- and anti-angiogenic, respectively. Although the angiogenic role of PPARγ remains ambiguous, it is a crucial regulator in autocrine and paracrine signaling of cancer-associated fibroblasts and tumor-associated macrophages/immune cells. Of note, angiopoietin-like 4 (ANGPTL4), a secretory protein encoded by a target gene of PPARs, triggers critical oncogenic processes such as inflammatory signaling, extracellular matrix derangement, anoikis resistance and metastasis, making it a potential drug target for cancer treatment. To conclude, PPARs in the tumor microenvironment exhibit oncogenic activities which are highly controversial and dependent on many factors such as stromal cell types, cancer types, and oncogenesis stages. Thus, the success of PPAR-based anticancer treatment potentially relies on innovative strategies to modulate PPAR activity in a cell type-specific manner.

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Peroxisome Proliferator-Activated Receptor Gamma Pro12Ala/C161T Genotypes and Risky Haplotype Altering Risk of Breast Cancer: A Turkish Case–Control Study

Cited by 3 publications

References 40 publications

Association between PPARγ, PPARGC1A, and PPARGC1B genetic variants and susceptibility of gastric cancer in an Eastern Chinese population

Association between PPARγ, PPARGC1A, and PPARGC1B genetic variants and susceptibility of gastric cancer in an Eastern Chinese population

Joint effects of PPARG-C161T (rs3856806) polymorphism and cardiovascular risk factors on restenosis risk after coronary stent implantation

PPARs and Tumor Microenvironment: The Emerging Roles of the Metabolic Master Regulators in Tumor Stromal–Epithelial Crosstalk and Carcinogenesis

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