Abstract
Peroxisome proliferator-activated receptor-γ2 gene Pro12Ala allele polymorphism (PPARG2 Pro12Ala; rs1801282) has been linked to both cancer risk and dietary factors. We conducted the first systematic literature review of studies published before December 2020 using the PubMed database to summarize the current evidence on whether dietary factors for cancer may differ by individuals carrying C (common) and/or G (minor) alleles of the PPARG2 Pro12Ala allele polymorphism. The inclusion criteria were observational studies that investigated the association between food or nutrient consumption and risk of incident cancer stratified by PPARG2 Pro12Ala allele polymorphism. From 3815 identified abstracts, nine articles (18,268 participants and 4780 cancer cases) covering three cancer sites (i.e., colon/rectum, prostate, and breast) were included. CG/GG allele carriers were more impacted by dietary factors than CC allele carriers. High levels of protective factors (e.g., carotenoids and prudent dietary patterns) were associated with a lower cancer risk, and high levels of risk factors (e.g., alcohol and refined grains) were associated with a higher cancer risk. In contrast, both CG/GG and CC allele carriers were similarly impacted by dietary fats, well-known PPAR-γ agonists. These findings highlight the complex relation between PPARG2 Pro12Ala allele polymorphism, dietary factors, and cancer risk, which warrant further investigation.
Highlights
Peroxisome proliferator-activated receptor-γ (PPARG or PPAR-γ) belongs to the nuclear hormone receptor superfamily, which induces target gene expression by binding as a heterodimer with retinoid X receptor alpha to PPAR-response element, the specific DNA motifs [1,2,3,4]
Several diet-derived and synthetic small lipophilic compounds can bind to PPARG and modify its activity, either fully or partially promoting, or completely inhibiting it [1,2,7]
Our systematic review included nine articles, which included a total of 18,268 participants with 4780 cancer cases from eight studies
Summary
Peroxisome proliferator-activated receptor-γ (PPARG or PPAR-γ) belongs to the nuclear hormone receptor superfamily, which induces target gene expression by binding as a heterodimer with retinoid X receptor alpha to PPAR-response element, the specific DNA motifs [1,2,3,4]. The three known splice variants of PPAR-γ include PPARG1, PPARG2, and PPARG3, with PPARG2 being the longest and most bioactive [5,6]. Several diet-derived and synthetic small lipophilic compounds can bind to PPARG and modify its activity, either fully or partially promoting, or completely inhibiting it [1,2,7]. PPAR-γ agonists are long- and very-long-chain fatty acids, and their derivatives and thiazolidinediones such as rosiglitazone and piaglitazone. They play a role in the PPAR-γ ’s most important metabolic function, which is to remove excess fatty acids and glucose from circulation through insulin signaling pathways [8]. Partial PPAR-γ agonists such as resveratrol, β-cryptoxanthine, 4.0/)
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