Latest Research: NMN Slowed Cancer Metastasis

This latest research has shown that NMN actually blunted the spread of an existing cancer.
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Links:
https://www.nature.com/articles/s41388-023-02592-y
https://pubmed.ncbi.nlm.nih.gov/36690678/
https://www.researchgate.net/publication/367342166_NAD_supplementation_limits_triple-negative_breast_cancer_metastasis_via_SIRT1-P66Shc_signaling
https://www.lifespan.io/news/nad-helps-natural-killer-cells-to-fight-cancer/
Jiang, Y., Luo, Z., Gong, Y. et al. NAD+ supplementation limits triple-negative breast cancer metastasis via SIRT1-P66Shc signaling. Oncogene (2023).
Yaku, K., Okabe, K., Hikosaka, K., & Nakagawa, T. (2018). NAD metabolism in cancer therapeutics. Frontiers in oncology, 8, 622.
Cantó, C., Menzies, K. J., & Auwerx, J. (2015). NAD+ metabolism and the control of energy homeostasis: a balancing act between mitochondria and the nucleus. Cell metabolism, 22(1), 31-53.
Kerksick, C., & Willoughby, D. (2005). The antioxidant role of glutathione and N-acetyl-cysteine supplements and exercise-induced oxidative stress. Journal of the international society of sports nutrition, 2(2), 38.
Porporato, P. E., Payen, V. L., Pérez-Escuredo, J., De Saedeleer, C. J., Danhier, P., Copetti, T., … & Sonveaux, P. (2014). A mitochondrial switch promotes tumor metastasis. Cell reports, 8(3), 754-766.

Like many bio-molecules, NAD+ is a double-edged sword, especially when looking into its self-contradictory relationship with cancer.
Note there that I said it was NAD that was the doubled edged sword, and not NMN. On the one hand, NAD+ is used as fuel by many types of cancer cells. And on the other hand, it can boosts an anti-cancer immune response. Other NAD-dependent enzymes such as the Sirtuins and PARP also seem to have a context-dependent effect on cancer. In this study researchers studied the effects of NAD+ on Triple-Negative Breast Cancer (TNBC). TNBC cells lack the three common receptors that are usually found on the surfaces of breast cancer cells, which limit the full array of therapeutic options that are usually open to doctors. The researchers initially generated primary tumors by injecting HCC1937 cancer cells, a common model of TNBC, into the mammary fat pads of immune-compromised mice. Continuous treatment with NMN significantly impeded tumor growth and cancer metastasis. Similar results were obtained using actual TNBC cells taken from a cancer patient. The researchers then proceeded to study NAD+ metabolism in vitro (meaning in glass, so outside of their normal biological context) and found that NMN supplementation rapidly increased intracellular NAD+ levels; as it usually does. While the treatment did not affect the proliferation of cancer cells, it slowed their migration and invasion. RNA sequencing of tumor samples revealed that NMN supplementation led to the activation of genes involved in longevity-regulating pathways and glutathione metabolism. It has been argued that Glutathione is probably the most important antioxidant that humans produce. Recent studies have shown that some protective effects of NAD+ might be attributed to its regulation of SIRT1, a member of the sirtuin family.
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