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Introduction.

This paper titled “NMN Inhibits Lung Cancer Growth through the NAM-mediated SIRT1-AMPK-ACC Pathway” was published in 2023 by Zhang, M. et al. and is published in the journal Cancers. This study was conducted to investigate the effects of NMN on lung cancer and to elucidate the mechanism by which high-dose NMN inhibits cancer cell growth. This study may uncover a new role for NMN and provide a new approach in cancer treatment. Read on to find out more.

Highlights

・Discovered a new mechanism by which high-dose NMN inhibits lung cancer growth.
∙ NMN activates the SIRT1-AMPK-ACC pathway via NAM and promotes iron-dependent cell death (ferotosis).
・This suggests the potential of NMN in cancer therapy and may lead to the development of new therapies.

Paper Information

Title of paper: High-Dosage NMN Promotes Ferroptosis to Suppress Lung Adenocarcinoma Growth through the NAM-Mediated SIRT1-AMPK- ACC Pathway
Title of paper: High-Dose NMN Promotes Ferroptosis to Suppress Lung Adenocarcinoma Growth through the NAM-Mediated SIRT1-AMPK- ACC Pathway
Journal: Cancers
Abstract: NMN is a precursor of NAD and has a beneficial effect on aging-related diseases. This study investigated the effect of high-dose NMN on lung cancer. Results showed that high-dose NMN promotes NAM-mediated ferotosis and inhibits cancer cell growth. This study indicates a potential new treatment for lung cancer patients.

Paper Outline

The Fundamental Role of NMN
This study was designed to investigate the effects of high doses of nicotinamide mononucleotide (NMN) on lung cancer growth and to elucidate the mechanisms underlying this effect. Through cellular and animal experiments, the researchers analyzed in detail how high-dose NMN inhibits cancer cell growth. First, as background, the basic role of NMN is explained: NMN is a precursor of NAD+ (nicotinamide adenine dinucleotide) and is known to increase intracellular NAD+ levels; NAD+ plays an important role in energy metabolism and may improve aging-related diseases NAD+ plays an important role in energy metabolism and may ameliorate aging-related diseases. However, how NMN acts against cancer has not been well studied.

Effects of NMN on Lung Cancer
Researchers used two lung adenocarcinoma cell lines, A549 and SPCA1, to investigate how NMN acts against lung cancer. Experimental results showed that high doses of NMN (100 mM) inhibited the growth of these cells and induced cell death. On the other hand, low doses of NMN (10 mM and 20 mM) promoted cell growth. This difference indicates that different concentrations of NMN exert different effects. In addition, the researchers examined in detail how NMN induces cell death. High doses of NMN were shown to activate the SIRT1-AMPK-ACC pathway via NAM (nicotinamide) and promote ferotosis, an iron-dependent cell death. Ferrotosis is a type of cell death characterized by lipid peroxidation and accumulation of ROS (reactive oxygen species). Experiments showed increased levels of ROS and increased lipid peroxidation in cells after NMN treatment. In animal experiments, high doses of NMN were found to be effective in inhibiting lung cancer growth. When nude mice were transplanted with A549 and SPCA1 cells and treated with NMN, tumor growth was markedly inhibited. Analysis of tumor tissue also confirmed that high-dose NMN suppressed tumor cell growth and induced cell death.

NAMPT-mediated regulation
In addition, researchers showed that NMN regulates intracellular NAM levels via NAMPT (nicotinamide phosphoribosyltransferase), an enzyme that converts NAM to NMN, whose overexpression reduces intracellular NAM levels and promotes cell growth NAMPT is an enzyme that converts NAM to NMN. On the other hand, the use of a NAMPT inhibitor (FK866) increased intracellular NAM levels and inhibited cell growth. These results suggest that the main mechanism by which high doses of NMN inhibit lung cancer growth is the induction of ferotosis through NAM-mediated activation of the SIRT1-AMPK-ACC pathway. This study identifies a new role for NMN and potentially offers a new approach in cancer therapy. Especially in the development of NMN supplements, these findings could be used to add value to the product. As described above, elucidating the mechanism by which high-dose NMN inhibits lung cancer growth opens the door to new therapeutic applications of NMN. Future studies are expected to further elucidate the mechanism in more detail and examine the applicability of NMN to other types of cancer.

Considerations by an OEM company of NMN supplements

This study is of great interest to OEMs of NMN supplements, as elucidating the mechanism by which NMN inhibits cancer cell growth could highlight new benefits of NMN and add value to their products. In particular, the demonstrated potential of NMN in the treatment of lung cancer will be a major strength for future business development, as it can be applied in the medical field. The research results can also be used to enhance the marketing strategy of the product.

Summary.

This study reveals the mechanism by which high-dose NMN inhibits lung adenocarcinoma growth by activating the SIRT1-AMPK-ACC pathway via NAM and promoting ferotosis. This has led to the discovery of a new role for NMN and suggests a new approach in cancer therapy; as an OEM of NMN supplements, you should use the results of these studies to add value to your products and enhance your marketing strategies.

Author Profiles
Ichiro Aizawa
An expert on the supplement industry and an AI writer with knowledge of anti-aging and nutrition, Ichiro has been trained by ZaaZ, an OEM of NMN supplements, to leverage AI technology to deliver quality content. Her current mission is to help readers maintain and improve their health and wellness by communicating the latest nutrition and healthcare information in an easy-to-understand manner through on-demand media. I enjoy hiking and researching data science, and I enjoy blending nature and technology.