Sesamin, a cancer chemopreventative

Molecular Cancer ResearchAs the authors of this paper published last month in Molecular Cancer Research state:

"Agents that are safe, affordable, and efficacious are urgently needed for the prevention of chronic diseases such as cancer."

They establish their rationale for investigating the sesame seed lignan called sesamin as a cancer chemopreventative:

"Sesamin...has been linked with prevention of hyperlipidemia, hypertension, and carcinogenesis through an unknown mechanism. Because the transcription factor NF-κB has been associated with inflammation, carcinogenesis, tumor cell survival, proliferation, invasion, and angiogenesis of cancer, we postulated that sesamin might mediate its effect through the modulation of the NF-κB pathway."

They found in fact that sesamin packs quite a punch:

"...sesamin inhibited the proliferation of a wide variety of tumor cells including leukemia, multiple myeloma, and cancers of the colon, prostate, breast, pancreas, and lung. Sesamin also potentiated tumor necrosis factor-α–induced apoptosis and this correlated with the suppression of gene products linked to cell survival, proliferation, inflammation (e.g., cyclooxygenase-2), invasion (e.g., matrix metalloproteinase-9, intercellular adhesion molecule 1), and angiogenesis (e.g., vascular endothelial growth factor). Sesamin downregulated constitutive and inducible NF-κB activation induced by various inflammatory stimuli and carcinogens..."

Those of you who may be pursuing immunopheresis for cancer (filtering TNF-α soluble receptors that barricade tumors from the immune system's attack) may very well wish to include sesamin in your protocol since it enhances cytotoxic TNF-α activity. Interestingly, sesamin is included in some of our omega-3 fatty acid formulae for brain support as an evidence-based agent for reducing brain inflammation. So the authors' conclusion is a welcome one:

"Overall, our results showed that sesamin may have potential against cancer and other chronic diseases through the suppression of a pathway linked to the NF-κB signaling."

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