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Editorial
. 2017 Sep 17;16(18):1635-1636.
doi: 10.1080/15384101.2017.1360633. Epub 2017 Aug 3.

Nicotinic acid: A case for a vitamin that moonlights for cancer?

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Editorial

Nicotinic acid: A case for a vitamin that moonlights for cancer?

Francesco Piacente et al. Cell Cycle. .
No abstract available

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Figures

Figure 1.
Figure 1.
Biosynthetic pathway of NAD+ production starting from Na. Nicotinic acid (Na) is converted to NAD+ through the 3-step Preiss-Handler pathway. NAPRT catalyzes the formation of nicotinic acid mononucleotide (NaMN) by adding a 5-phosphoribose group (P-ribose) from 5-phosphoribosyl-1-pyrophosphate to Na. NaMN is converted to nicotinic acid adenine dinucleotide (NaAD+) by nicotinamide mononucleotide adenylyltransferase 1/3 (NMNAT1–3). Finally, NAD+ synthase 1 (NADSYN1) converts NaAD+ to NAD+. The NAPRT gene is amplified and overexpressed in a subset of tumors, including ovarian, breast, pancreatic and prostate cancer. NAPRT-derived NAD+ supports the activity of DNA repair enzymes, such as PARP1/2, which, in turn, may be especially important in cancer cells with defective homologous recombination DNA repair to avoid catastrophic DNA damage. In addition, NAPRT-mediated NAD+ production turns out to be especially important for replenishing the mitochondrial NAD+ stores, for promoting OXPHOS, ATP synthesis, and protein synthesis and, ultimately, for regulating cell size. PAR: poly (ADP-ribose).

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References

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