Methyl Donors Inhibit Panc-1 Cell Proliferation by Decreasing NFkB and Erk Signaling Levels and Raising E-Cadherin Expression

Kiss, Eva and Forika, Gertrud and Takacs, Istvan and Krenacs, Tibor and Nemeth, Zsuzsanna (2022) Methyl Donors Inhibit Panc-1 Cell Proliferation by Decreasing NFkB and Erk Signaling Levels and Raising E-Cadherin Expression. In: Current Practice in Medical Science Vol. 8. B P International, pp. 119-141. ISBN 978-93-5547-752-1

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We hypothesized that dietary methyl-donors may improve the physiology of cancer patients including those with pancreatic cancer, and could be used for intervention therapy. In this study, methyl-donor treatment (L-methionine, choline chloride, folic acid and vitamin B12) of an aggressive pancreatic adenocarcinoma cell line (Panc-1) resulted in significantly increased p21WAF1/Cip1 cyclin dependent kinase inhibitor levels along with the apoptotic SubG1 fractions and at the same time, phospho-Erk1/2 levels and the proliferation rate were significantly reduced. An aggressive cancer with a high risk of metastasizing like pancreatic cancer, diet is one of the lifestyle-related variables in its genesis. Methyl-donors are dietary micronutrients that support key metabolic pathways and operate as bioactive food components by supplying methyl groups as cofactors and substrates. Imbalanced nutritional status of methyl-donors has recently been linked to pathological conditions. Though methyl donor treatments also increased the pro-apoptotic protein Bak, Puma and Caspase-9, failed to elevate cleaved Caspase-3 levels. In addition, the treatment significantly reduced the production of the pro-inflammatory cytokine IL-17a and the transcription factor NFkB. SDF-1a and VEGF levels were found to be significantly lower after methyl-donor treatmtnts, which may signify a decreased risk of metastatic spread. E-cadherin expression increased after the methyl-donor therapy, as was predicted, and was inversely related to these alterations. It is concluded that methyl-donors may have the potential to reduce aggressive and proliferative phenotype of Panc-1 cells. This suggests a promising role of dietary methyl-donors for complementing relevant cancer therapies even in treatment resistant pancreatic adenocarcinomas.

Item Type: Book Section
Subjects: Eprints AP open Archive > Medical Science
Depositing User: Unnamed user with email
Date Deposited: 16 Oct 2023 04:09
Last Modified: 16 Oct 2023 04:09

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