Dietary patterns in association with the expression of pro-metastatic genes in primary breast cancer

Metastasis is a major leading cause of mortality in female breast cancer (BrCa). Cellular motility is a pathological process of metastasis remarked by the overexpression of cortactin (CTTN), Ras homolog family member-A (RhoA), and Rho-associated kinase (ROCK) genes. Their balance is responsible for upholding the integrity of healthy epithelial cell junctions. This study aimed to explore the associations between a posteriori dietary patterns and the expression levels of pro-metastatic genes in primary BrCa.

In this consecutive case series, 215 eligible women, newly diagnosed with histologically confirmed non-metastatic BrCa (stage I-IIIA), were recruited from Hospitals in Tabriz, Northwestern Iran (2015-2017). The tumoral expression levels of genes were quantified using real-time reverse transcription-polymerase chain reaction. Dietary data assessment was carried out using a validated food frequency questionnaire.

Three dietary patterns were identified using principal component analysis (KMO = 0.699). Adherence to the "vegan" pattern (vegetables, fruits, legumes, nuts, seeds, and whole grains) was inversely associated with the expression levels of RhoA (OR_Adj.T3vs.T1 = 0.24, 95%CI 0.07-0.79) and ROCK (OR_Adj.T3vs.T1 = 0.26, 95%CI 0.08-0.87). In addition, the highest adherence to the "prudent" pattern (spices, seafood, dairy, and vegetable oils) decreased the odds of overexpressions at RhoA (OR_Adj.T3vs.T1 = 0.26, 95%CI 0.08-0.84) and ROCK genes (OR_Adj.T3vs.T1 = 0.29, 95%CI 0.09-0.95). The highest adherence to "Western" pattern (meat, processed meat, hydrogenated fat, fast food, refined cereals, sweets, and soft drinks) was a risk factor associated with the overexpression of RhoA (OR_Adj.T3vs.T1 = 3.15, 95%CI 1.12-8.85).

Adherence to healthy dietary patterns was significantly associated with the downregulation of pro-metastatic genes. Findings provided new implications to advance the nutrigenomic knowledge to prevent the odds of over-regulations in pro-metastatic genes of the primary BrCa.