Table 1 Summary of the effects of nutrients on breast cancer-related genes
From: Interactions dietary components with expression level of breast cancer-related genes
Author (year) | Nutrients | Cancer-related gene | Design | The mechanism of effect |
|---|---|---|---|---|
Kim et al. [36] | Folic acid | BRCA1 | Case–control | The moderate use of folic acid can prevent DNA strand breaks, chromosomal inconsistency, impaired DNA repair, and neoplastic transformation, in particular in a person who has inherited a mutation of BRCA |
Kim et al. [36] | Vitamin B12 | BRCA1 | Case–control | Protective effect by several mechanisms such as participating in synthesis, repair, and methylation of DNA and also preventing aggregation Uracil and chromosome breaks |
Romagnolo et al. [38] | Genistein | BRCA1 | Experimental | Protective effect by several mechanisms such as rescued BRCA-1 protein expression, reduced DNMT-1, and cyclin D1, reduced BRCA1 CpG methylation, and reduced cell proliferation associated with increased p53 level |
Pickholtz et al. [39] | Vitamin D | BRCA1 | Experimental | It is similar to BRCA1. Vitamin D receptor (VDR) and vitamin D responsive elements (VDRE) are co-occupied by BRCA1 at the CDKN1A promoter (p21waf1), where acetylation of H3 and H4 is increased |
Baumann et al. [41] | Exogenous palmitat | HER2 | Experimental | Protective effect by several mechanisms such as inducing ER stress response through the activation of IRE1 and ATF6 that accompany with a reduction in HER2 and HER3 protein levels, increasing in DDIT3/CHOP expression that causes cell death, sensitizing HER2-positive breast cancer cells in trastuzumab treatment |
Olive oil | HER2 | Experimental | Olive oil had a protective effect by several mechanisms such as suppressing HER-2 expression and increasing the trastuzumab efficacy by oleic acid of olive oil, inducing apoptotic cell death, and synergistically enhancing trastuzumab-efficacy by Oleuropein aglycone phenol of olive oil | |
Alpha-linolenic acid | HER2 | Experimental & RCT | The molecular mechanism by which ALA inhibits breast cancer cell growth and metastasis formation may involve suppressing the overexpression of HER2 | |
Mason [45] | Flaxseed oil | HER2 | Experimental | Tumorigenesis is inhibited by flaxseed oil and growth factor receptor signaling pathways are modulated. Its protective mechanisms include reducing the expression of other growth factor receptors, such as EGFR and IGF-IR, as well as reducing the activity of FASN and enhancing the expression of the tumor suppressor PTEN |
Zabaleta [48] | Epigallocatechin-gallate | HER2 | Systematic review | Several mechanisms are responsible for this protective effect, such as inducing apoptosis and inhibiting cell proliferation |
Genistein | HER2 | Systematic review & Experimental | Genistein inhibits the growth of cells by deregulating HER2 | |
Zabaleta [48] | Kaempferol | HER2 | Systematic review | This protective effect is due to several mechanisms such as cell cycle arrest and apoptosis, which are correlated with phosphorylated p53 upregulation |
Zabaleta [48] | Resveratrol | HER2 | Systematic review | By inhibiting FASN signaling and downregulating HER2 and p185HER2/neu, resveratrol inhibits proliferation |
Doaei et al. [53] | Carbohydrate | FTO | Systematic review of experimental studies | High levels of blood glucose and insulin can worsen the risk of cancer by activation of phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway Also, higher glucose intake up-regulated FTO gene expression |
Doaei et al. [53] | protein | FTO | Population-based trial | Protein intake significantly upregulated the FTO gene |
Yadav et al. [57] | B12 | FTO | cohort | B12 supplementation can influence the regulation of FTO through methylation of miR21 |