Next Article in Journal
Melatonin Attenuates Pulmonary Hypertension in Chronically Hypoxic Rats
Next Article in Special Issue
Gene-Diet Interactions in Type 2 Diabetes: The Chicken and Egg Debate
Previous Article in Journal
The Cytokine Flt3-Ligand in Normal and Malignant Hematopoiesis
Previous Article in Special Issue
NutrimiRAging: Micromanaging Nutrient Sensing Pathways through Nutrition to Promote Healthy Aging
Article Menu
Issue 6 (June) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2017, 18(6), 1116;

Molecular Basis of Alcohol-Related Gastric and Colon Cancer

Department of Food Science and Biotechnology, College of Knowledge-Based Services Engineering, Sungshin Women’s University, Seoul 01133, Korea
Author to whom correspondence should be addressed.
Academic Editors: Lynnette Ferguson and Virginia R. Parslow
Received: 27 March 2017 / Revised: 4 May 2017 / Accepted: 6 May 2017 / Published: 24 May 2017
(This article belongs to the Special Issue Gene-Diet Interactions in Chronic Diseases)
Full-Text   |   PDF [771 KB, uploaded 24 May 2017]   |  


Many meta-analysis, large cohort studies, and experimental studies suggest that chronic alcohol consumption increases the risk of gastric and colon cancer. Ethanol is metabolized by alcohol dehydrogenases (ADH), catalase or cytochrome P450 2E1 (CYP2E1) to acetaldehyde, which is then further oxidized to acetate by aldehyde dehydrogenase (ALDH). Acetaldehyde has been classified by the International Agency for Research on Cancer (IARC) as a Group 1 carcinogen to humans. The acetaldehyde level in the stomach and colon is locally influenced by gastric colonization by Helicobacter pylori or colonic microbes, as well as polymorphisms in the genes encoding tissue alcohol metabolizing enzymes, especially ALDH2. Alcohol stimulates the uptake of carcinogens and their metabolism and also changes the composition of enteric microbes in a way to enhance the aldehyde level. Alcohol also undergoes chemical coupling to membrane phospholipids and disrupts organization of tight junctions, leading to nuclear translocation of β-catenin and ZONAB, which may contributes to regulation of genes involved in proliferation, invasion and metastasis. Alcohol also generates reactive oxygen species (ROS) by suppressing the expression of antioxidant and cytoprotective enzymes and inducing expression of CYP2E1 which contribute to the metabolic activation of chemical carcinogens. Besides exerting genotoxic effects by directly damaging DNA, ROS can activates signaling molecules involved in inflammation, metastasis and angiogenesis. In addition, alcohol consumption induces folate deficiency, which may result in aberrant DNA methylation profiles, thereby influencing cancer-related gene expression. View Full-Text
Keywords: alcohol; acetaldehyde; gastric cancer; colon cancer; polymorphism; reactive oxygen species alcohol; acetaldehyde; gastric cancer; colon cancer; polymorphism; reactive oxygen species

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Na, H.-K.; Lee, J.Y. Molecular Basis of Alcohol-Related Gastric and Colon Cancer. Int. J. Mol. Sci. 2017, 18, 1116.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top