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Epigenetics, Alcohol, and Cancer

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Alcohol and Cancer

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Abstract

Chronic or excessive alcohol consumption often leads to various medical disorders, including liver cirrhosis, pancreatitis, cardiomyopathy, fetal abnormalities, brain damage, and various cancers. To effectively prevent or treat these disorders, a better understanding of their underlying mechanisms is pivotal. Alcohol and its metabolites alter cellular functions through changes at the levels of DNA, RNA, protein, and metabolites, resulting in pathophysiological changes. Although the amount of RNA, protein, or metabolites is determined by dynamic processes of synthesis and degradation with many regulators involved, it is initially predominantly determined by the activity of the genes involved. Two major mechanisms of gene regulation involve genetic and epigenetic controls of gene expression. In the past half century, research and technological innovations have led to a remarkable progress in understanding the genetic controls of gene activities. However, only in recent years, epigenetic controls of gene expression drew immense interest, especially in the biomedical fields of cancer and ageing. To date, research efforts to understand effects of alcohol on regulation of gene activity have been primarily focused on genetic factors. The mechanisms of epigenetic modifications in alcohol-induced organ damage, including cancers, have only started to be tackled in the past few years.

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Abbreviations

CpG:

Cytosine-guanine dinucleotide

DNMT:

DNA methyl transferase

ER:

Endoplasmic reticulum

GSH:

Glutathione

GST:

Glutathione S-transferase

HAT:

Histone acetyltransferase

HCC:

Hepatocellular carcinoma

HDAC:

Histone deacetylase

HERP:

Homocysteine-induced endoplasmic reticulum protein

HMT:

Histone methyltranferase

HNSCC:

Head and neck squamous cell carcinoma

JAK:

Janus kinase

MAP kinase:

Mitogen-activated protein kinase

MAT:

Methionine adenosyltransferase

miRNA:

microRNA

MTHFR:

Methylene tetrahydrofolate reductase

NAD and NADH:

Oxidized and reduced nicotinamide adenine dinucleotide, respectively

ncRNA:

Nonprotein-coding RNA

PLP:

Pyridoxal-5′ phosphate

RISC:

RNA-induced silencing complex

RITS:

RNA-induced transcriptional silencing

SAH:

S-adenosyl-homocysteine

SAM (or SAMe):

S-adenosylmethionine

STAT:

Signal transducer and activator of transcription

TGS:

Transcriptional gene silencing

THF:

Tetrahydrofolate

UTRs:

Untranslated regions

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Authors and Affiliations

  1. Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA

    Dale Hereld MD, PhD & Q. Max Guo PhD

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  1. Dale Hereld MD, PhD
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Correspondence to Dale Hereld MD, PhD .

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  1. , Division of Metabolism and Health Effect, National Institute on Alcohol Abuse and, 5635 Fishers Lane, Room 2031, Bethesda, 20892-9304, Maryland, USA

    Samir Zakhari

  2. , Deparment of Pharmaceutical Sciences, University of Colorado Denver, 12700 East 19th Ave, Aurora, 80045, Colorado, USA

    Vasilis Vasiliou

  3. , Division of Metabolism and Health Effect, National Institute on Alcohol Abuse and, 5635 Fishers Lane, Room 2031, Bethesda, 20892-9304, Maryland, USA

    Q. Max Guo

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Hereld, D., Guo, Q.M. (2011). Epigenetics, Alcohol, and Cancer. In: Zakhari, S., Vasiliou, V., Guo, Q. (eds) Alcohol and Cancer. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-0040-0_5

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