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1. Introduction
From current studies on human whole genomes, we have already learned that “cancer is a genetic disease” after understanding the genomic/genetic differences between cancer and normal cells through next-generation sequencing [1,2]. At present, whole-genome sequencing data can predict the incidence of specific diseases, including cancer, in healthy individuals [3]. However, recent metabolome studies suggest that metabolites could be biomarkers for cancer and its development [4], suggesting as well that “cancer is a metabolic disease”. It is well known that cancer mainly uses glucose to produce adenosine triphosphate (ATP) by glycolysis. The “Warburg effect”, or abnormal metabolism, which was described by Dr. Otto Warburg over 60 years ago, is widely known as one of the most essential characteristics in cancer cells [5,6,7]. Importantly, it is frequently observed that both dysregulation of the tricarboxylic acid (TCA) cycle (Krebs/Citrate cycle) and oxidative phosphorylation occur in cancer cells, suggesting that mitochondrial dysfunction precedes the metabolic change [8], indicating that “cancer is a mitochondrial disease”. Mitochondria have their own DNA or mitochondrial DNA (mtDNA), suggesting that they have evolved from the symbiosis of aerobic bacteria (α-proteobacteria) into ancestral eukaryotic cells. However, it should be noted that most (99%) of the genes that encode mitochondrial function-associated proteins are contained in nuclear genomes [9]. Therefore, mitochondrial function-associated genes are commonly regulated by transcription factors (TFs) that regulate other cellular protein-encoding genes.
In this regard, scientific interest should be focused on causative factors that lead to mitochondrial dysfunction by asking whether “cancer could be a transcriptional disease”. In this chapter, through a discussion mainly about biological functions and regulations of nicotinamide adenine dinucleotide (NAD+), which is not only required as a co-enzyme for various biologically significant reactions but also as a substrate for poly (ADP-ribose) polymerase (PARP), we propose a novel anti-cancer therapy that converts or forces cancerous cells to return to a non-proliferating or differentiated state.
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Edited by Nigeria Custom Officer, 08 March 2020 - 10:57 AM.
