Abstract

In the Western Countries, colon cancer is the third tumor for aggressiveness and incidence after lung andbreast/prostate cancer. Different risk factors concur to the development of colon cancer, including geneticfactors, inflammation, intestinal microflora composition, as well as lifestyle. Epidemiologic studiescorrelating alcohol consumption and assert that the risks are 5-fold higher amongdrinkers compared to nondrinkers. However, the exact mechanisms correlating heavy alcohol drinking andcolon cancer are not completely elucidated yet. To shed light on the biochemical mechanisms through whichalcohol favors colon cancer progression, we evaluated the effect of high doses of ethanol (100 mM and 300mM) on HCT116 and HT29 cells, two human colon cancer cell lines. Our study provided evidence thatethanol did not exert cytotoxic effects on either the cell lines, but rather promoted cell survival andproliferation. Western blot analyses showed that ethanol exposure increased the level of GRP78 and Chop,two markers of endoplasmic reticulum stress. Furthermore our analysis demonstrated that ethanol promotedthe autophagy as a defense mechanism and induced activation of Nrf2, the main regulator of anti-oxidantresponse. These defense mechanisms were correlated with an increase in the metalloprotease activity,making the colon cancer cell phenotype more invasive.
Lingua originaleEnglish
Titolo della pubblicazione ospiteEthanol promotes survival and tumor progression of colon cancer cells
Numero di pagine1
Stato di pubblicazionePublished - 2018

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Colonic Neoplasms
Ethanol
Survival
Defense Mechanisms
Neoplasms
Alcohol Drinking
HCT116 Cells
Cell Line
HT29 Cells
Endoplasmic Reticulum Stress
Autophagy
Metalloproteases
Life Style
Prostatic Neoplasms
Cell Survival
Western Blotting
Inflammation
Phenotype
Lung
Incidence

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@inproceedings{4bd1b110075b4916b20031485bbf0b81,
title = "Ethanol promotes survival and tumor progression of colon cancer cells",
abstract = "In the Western Countries, colon cancer is the third tumor for aggressiveness and incidence after lung andbreast/prostate cancer. Different risk factors concur to the development of colon cancer, including geneticfactors, inflammation, intestinal microflora composition, as well as lifestyle. Epidemiologic studiescorrelating alcohol consumption and assert that the risks are 5-fold higher amongdrinkers compared to nondrinkers. However, the exact mechanisms correlating heavy alcohol drinking andcolon cancer are not completely elucidated yet. To shed light on the biochemical mechanisms through whichalcohol favors colon cancer progression, we evaluated the effect of high doses of ethanol (100 mM and 300mM) on HCT116 and HT29 cells, two human colon cancer cell lines. Our study provided evidence thatethanol did not exert cytotoxic effects on either the cell lines, but rather promoted cell survival andproliferation. Western blot analyses showed that ethanol exposure increased the level of GRP78 and Chop,two markers of endoplasmic reticulum stress. Furthermore our analysis demonstrated that ethanol promotedthe autophagy as a defense mechanism and induced activation of Nrf2, the main regulator of anti-oxidantresponse. These defense mechanisms were correlated with an increase in the metalloprotease activity,making the colon cancer cell phenotype more invasive.",
author = "Antonella D'Anneo and {Lo Galbo}, Valentina and Giuseppe Calvaruso and Sonia Emanuele and Daniela Carlisi and Marianna Lauricella and Cesare Cernigliaro and Michela Giuliano",
year = "2018",
language = "English",
isbn = "9788894370706",
booktitle = "Ethanol promotes survival and tumor progression of colon cancer cells",

}

TY - GEN

T1 - Ethanol promotes survival and tumor progression of colon cancer cells

AU - D'Anneo, Antonella

AU - Lo Galbo, Valentina

AU - Calvaruso, Giuseppe

AU - Emanuele, Sonia

AU - Carlisi, Daniela

AU - Lauricella, Marianna

AU - Cernigliaro, Cesare

AU - Giuliano, Michela

PY - 2018

Y1 - 2018

N2 - In the Western Countries, colon cancer is the third tumor for aggressiveness and incidence after lung andbreast/prostate cancer. Different risk factors concur to the development of colon cancer, including geneticfactors, inflammation, intestinal microflora composition, as well as lifestyle. Epidemiologic studiescorrelating alcohol consumption and assert that the risks are 5-fold higher amongdrinkers compared to nondrinkers. However, the exact mechanisms correlating heavy alcohol drinking andcolon cancer are not completely elucidated yet. To shed light on the biochemical mechanisms through whichalcohol favors colon cancer progression, we evaluated the effect of high doses of ethanol (100 mM and 300mM) on HCT116 and HT29 cells, two human colon cancer cell lines. Our study provided evidence thatethanol did not exert cytotoxic effects on either the cell lines, but rather promoted cell survival andproliferation. Western blot analyses showed that ethanol exposure increased the level of GRP78 and Chop,two markers of endoplasmic reticulum stress. Furthermore our analysis demonstrated that ethanol promotedthe autophagy as a defense mechanism and induced activation of Nrf2, the main regulator of anti-oxidantresponse. These defense mechanisms were correlated with an increase in the metalloprotease activity,making the colon cancer cell phenotype more invasive.

AB - In the Western Countries, colon cancer is the third tumor for aggressiveness and incidence after lung andbreast/prostate cancer. Different risk factors concur to the development of colon cancer, including geneticfactors, inflammation, intestinal microflora composition, as well as lifestyle. Epidemiologic studiescorrelating alcohol consumption and assert that the risks are 5-fold higher amongdrinkers compared to nondrinkers. However, the exact mechanisms correlating heavy alcohol drinking andcolon cancer are not completely elucidated yet. To shed light on the biochemical mechanisms through whichalcohol favors colon cancer progression, we evaluated the effect of high doses of ethanol (100 mM and 300mM) on HCT116 and HT29 cells, two human colon cancer cell lines. Our study provided evidence thatethanol did not exert cytotoxic effects on either the cell lines, but rather promoted cell survival andproliferation. Western blot analyses showed that ethanol exposure increased the level of GRP78 and Chop,two markers of endoplasmic reticulum stress. Furthermore our analysis demonstrated that ethanol promotedthe autophagy as a defense mechanism and induced activation of Nrf2, the main regulator of anti-oxidantresponse. These defense mechanisms were correlated with an increase in the metalloprotease activity,making the colon cancer cell phenotype more invasive.

UR - http://hdl.handle.net/10447/364570

M3 - Conference contribution

SN - 9788894370706

BT - Ethanol promotes survival and tumor progression of colon cancer cells

ER -