Certain genes interact with total folate consumption and impact colorectal cancer risk

A recent study found evidence that suggested gene expression may interact with folate consumption to alter colorectal cancer (CRC) risk. The results of this study were published in Scientific Reports.

The study aimed to investigate interactions between folate consumption and predicted gene expression on colorectal cancer risk across the genome. For genes including glutathione S-Transferase Alpha 1 (GSTA1), Tonsuko Like, DNA Repair Protein (TONSL), and Aspartylglucosaminidase (AGA), hints of an association between folate consumption and CRC risk were observed.

For a set-based gene–environment (G × E) approach, variant weights from the PrediXcan models of colon tissue-specific gene expression as a priori variant information was used. Between cohort and case-control studies, the total folate intake (mcg/day) was harmonised based on dietary intake and supplementary use, and sex and study-specific quantiles were determined. Analyses was performed using a mixed effects score tests for interactions between folate and genetically predicted expression of 4839 genes and results were pooled from across 23 studies.

Three genes that may interact with folate consumption to change the risk of CRC were discovered by data pointing to possible interactions. Glutathione is an antioxidant, preventing cellular damage and is a downstream metabolite of homocysteine and metabolized by GSTA1. TONSL is part of a complex that functions in the recovery of double strand breaks and AGA plays a role in lysosomal breakdown of glycoprotein.

Hence, the three genes, GSTA1, TONSL and AGA may interact with folate consumption to alter colorectal cancer (CRC) risk.

Reference :

• Cameron B. Haas, Yu-Ru Su, Paneen Petersen, et. al. Interactions between folate intake and genetic predictors of gene expression levels associated with colorectal cancer risk. 2022 Nov. Scientific Reports. Nature.6 https://www.nature.com/articles/s41598-022-23451-y