The physiology of cancer patients, particularly those with pancreatic cancer, may be improved by dietary methyl donors, which may also be utilised as intervention treatment. In this study, an aggressive pancreatic adenocarcinoma cell line (Panc-1) was treated with methyl-donors (L-methionine, choline chloride, folic acid, and vitamin B12), which significantly increased the levels of p21WAF1/Cip1 cyclin dependent kinase inhibitor and the SubG1 fractions while significantly decreasing the levels of phospho-Erk1/2 and the proliferation rate. Diet is one of the lifestyle-related factors in the genesis of pancreatic cancer, an aggressive malignancy with a high chance of metastasizing. Methyl-donors are dietary micronutrients that function as bioactive food ingredients by delivering methyl groups as cofactors and substrates for critical metabolic pathways. Pathological disorders have recently been related to methyl-donors’ unbalanced nutritional status. Although Bak, Puma, and Caspase-9 levels were likewise raised by methyl donor treatments, cleaved Caspase-3 levels were not. The production of the transcription factor NFkB and the pro-inflammatory cytokine IL-17a was also markedly decreased by the therapy. After methyl-donor treatments, SDF-1a and VEGF levels were found to be much lower, which may indicate a reduced risk of metastatic dissemination. As was anticipated, E-cadherin expression increased following the methyl-donor therapy and was negatively correlated with these changes. It is determined that methyl-donors may have the ability to lessen Panc-1 cells’ aggressive and proliferative character. This implies a potential function for dietary methyl-donors in enhancing

Author (s) Details

Eva Kiss

Department of Internal Medicine and Oncology, Oncology Profile, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

Gertrud Forika

Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, 1085 Ulloi u 26, Hungary.0

Istvan Takacs

Department of Internal Medicine and Oncology, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

Tibor Krenacs

Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, 1085 Ulloi u 26, Hungary.

Zsuzsanna Nemeth

Department of Internal Medicine and Oncology, Semmelweis University, Budapest, 1083 Budapest Koranyi S u 2/a, Hungary.

Please see the link here:-  https://stm.bookpi.org/CPMS-V8/article/view/7800

Keywords –  Methyl-donors, cell cycle, apoptosis, E-cadherin, metastatic potential