Key result
Targeting NNMT and supplementing 1-MNA may prevent cancer-associated thrombosis and affect carcinogenesis.
Targeting nicotinamide N-methyl transferase (NNMT) and supplementing with 1-MNA may offer a novel approach to preventing cancer-associated thrombosis.
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May support NNMT inhibition trials in cancer-associated thrombosis; leaves open clinical efficacy and safety.
Nicotinamide metabolism is important in carcinogenesis. Nicotinamide affects the cellular methyl pool, thus affecting DNA and histone methylation and gene expression. Cancer cells have increased expression of nicotinamide N-methyl transferase (NNMT), the key enzyme in nicotinamide metabolism. NNMT contributes to tumor angiogenesis. Overexpression of NNMT is associated with poorer prognosis in cancers. Additionally, NNMT can contribute to cancer-associated morbidities, such as cancer-associated thrombosis. 1-methylnicotinamide (1-MNA), a metabolite of nicotinamide, has anti-inflammatory and antithrombotic effects. Therefore, targeting NNMT can affect both carcinogenesis and cancer-associated morbidities. Several antitumor drugs have been shown to inhibit NNMT expression in cancer cells. Implementing these drugs to reverse NNMT effects in addition to 1-MNA supplementation has the potential to prevent cancer-associated thrombosis through various mechanisms.
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Jabbari et al. (2023) conducted a review in Cancer-associated thrombosis. NNMT inhibitors and 1-MNA supplementation was evaluated. Targeting nicotinamide N-methyl transferase (NNMT) and supplementing 1-methylnicotinamide (1-MNA) has the potential to prevent cancer-associated thrombosis and affect carcinogenesis.
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