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Insight Into Nicotinamide Adenine Dinucleotide Homeostasis as a Targetable Metabolic Pathway in Colorectal Cancer. | LitMetric

AI Article Synopsis

  • Tumor cells adapt their metabolism to support uncontrolled growth by requiring sufficient levels of NAD and NADPH.
  • *NAD is a key cofactor for important enzymes like PARPs and sirtuins, while NADPH helps regulate cellular redox status.
  • *The review discusses strategies for targeting the enzymes that sustain the NAD/NADPH pool in colorectal cancer and how these enzymes interact with NADP(H).

Article Abstract

Tumour cells modify their cellular metabolism with the aim to sustain uncontrolled proliferation. cells necessitate adequate amounts of NAD and NADPH to support several enzymes that are usually overexpressed and/or overactivated. Nicotinamide adenine dinucleotide (NAD) is an essential cofactor and substrate of several NAD-consuming enzymes, such as PARPs and sirtuins, while NADPH is important in the regulation of the redox status in cells. The present review explores the rationale for targeting the key enzymes that maintain the cellular NAD/NADPH pool in colorectal cancer and the enzymes that consume or use NADP(H).

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8645963PMC
http://dx.doi.org/10.3389/fphar.2021.758320DOI Listing

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