Regulatory roles of NAMPT and NAD+ metabolism in uterine leiomyoma progression: Implications for ECM accumulation, stemness, and microenvironment

Yi-Fen Chiang, Ko‐Chieh Huang, Tsui‐Chin Huang, Y-H. Chen, Mohamed Ali, Ayman Al-Hendy, Pei-Shen Huang, Shih‐Min Hsia
In: Redox Biology · 2024 · vol. 78 , pp. 103411 · doi:10.1016/j.redox.2024.103411 · PMID:39486360 · W4403820133
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This study found that elevated NAMPT and NAD+ metabolism contribute to uterine leiomyoma progression through ECM accumulation and stemness, and that NAMPT inhibitors like FK866 and NAM can suppress tumor growth.

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Abstract

Uterine leiomyoma (UL), commonly referred to as benign tumors, is characterized by excessive cell proliferation, extracellular matrix (ECM) accumulation, and the presence of stem cell-like properties. Nicotinamide adenine dinucleotide (NAD + ) metabolism, regulated in part by nicotinamide phosphoribosyltransferase (NAMPT), plays a crucial role in these pathological processes and has emerged as a potential therapeutic target. Additionally, redox signaling pathways are integral to the pathogenesis of UL, influencing the dynamics of NAD + metabolism. This study sought to elucidate the regulatory functions of NAMPT and NAD + metabolism, in conjunction with redox signaling, in the progression of UL, and to explore potential therapeutic strategies targeting these pathways. Evaluation of NAMPT expression in human UL tissues revealed a positive correlation between elevated NAMPT levels and increased ECM deposition, as well as the expression of stemness markers. The use of FK866 and nicotinamide (NAM), to inhibit NAMPT significantly suppressed UL cell viability and attenuated stem cell-like characteristics. Redox signaling pathways, including those associated with DNA damage, lysosomal function homeostasis, and redox-sensitive phagophore formation, were implicated in the regulation of ECM dynamics, particularly through ECM-targeted inhibition. This study highlights the pivotal roles of NAMPT, NAD + metabolism, and redox signaling in the pathophysiology of UL. Targeting NAMPT, particularly through the use of inhibitors FK866 and NAM, represents a promising therapeutic approach for mitigating UL progression by modulating redox and ECM dynamics. These findings offer novel insights into UL pathogenesis and establish NAMPT as a compelling target for future clinical investigation.

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