Alcohol, stem cells and cancer

Gu, Shoujun; Nguyen, Bao Ngoc; Rao, Shuyun; Li, Shulin; Shetty, Kirti; Rashid, Asif; Shukla, Vivek; Deng, Chu Xia; Mishra, Lopa; Mishra, Bibhuti

doi:10.18632/genesandcancer.156

Cited by 10 publications

(14 citation statements)

References 76 publications

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“…The incidence of hepatocellular carcinoma (HCC) has been increasing worldwide owing in part to extrinsic factors such as chronic liver disease caused by viral infections, alcohol and nonalcoholic fatty liver disease 1 – 4 . HCC is also associated with a high mortality because of its prolific rate of recurrence and heterogeneity, which has been attributed to the existence of cancer stem cells (CSCs) 5 .…”

Section: Introductionmentioning

confidence: 99%

CPEB1 mediates hepatocellular carcinoma cancer stemness and chemoresistance

Fang

Shen

et al. 2018

Cell Death Dis

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Cancer stem cells (CSCs) are a subpopulation of cells within tumors that are believed to possess pluripotent properties and thought to be responsible for tumor initiation, progression, relapse and metastasis. Cytoplasmic polyadenylation element-binding protein 1 (CPEB1), a sequence-specific RNA-binding protein that regulates mRNA polyadenylation and translation, has been linked to cancer progression and metastasis. However, the involvement of CPEB1 in hepatocellular carcinoma (HCC) remains unclear. In this study, we have demonstrated that CPEB1 directly regulates sirtuin 1 (SIRT1) mRNA to mediate cancer stemness in HCC. Cancer stemness was analyzed by self-renewal ability, chemoresistance, metastasis, expression of stemness-related genes and CSC marker-positive cell populations. The results indicate that CPEB1 is downregulated in HCC. Overexpression of CPEB1 dramatically reduced HCC cell stemness, whereas silencing CPEB1 enhances it. Using site-directed mutagenesis, a luciferase reporter assay, and immunoprecipitation, we found that CPEB1 could directly target the 3′-UTR of SIRT1, control poly(A) tail length and suppress its translation to mediate cancer stemness in vitro and in vivo. Overall, our findings suggest that the negative regulation between CPEB1 and SIRT1 contributes to the suppression of cancer stemness in HCC. CPEB1 may have potential as a therapeutic target in HCC.

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Section: Introductionmentioning

confidence: 99%

CPEB1 mediates hepatocellular carcinoma cancer stemness and chemoresistance

Fang

Shen

et al. 2018

Cell Death Dis

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“…Fanconi anemia and transforming growth factor β pathways are involved in the maintenance/differentiation of stem cells and alcohol metabolization [15]. The tumor suppressor β2-spectrin increased the tumor suppression mediated by the transforming growth factor β [279]. Both β2-spectrin and transforming growth factor β pathways, by controlling the Fanconi anemia DNA repair pathway, are involved in the genomic stability maintenance from genotoxic metabolites.…”

Section: Alcohol Cancer Stem Cells Theories and Therapeutic Strategiesmentioning

confidence: 99%

“…Both β2-spectrin and transforming growth factor β pathways, by controlling the Fanconi anemia DNA repair pathway, are involved in the genomic stability maintenance from genotoxic metabolites. β2-spectrin keeps this stability after alcohol-induced DNA damage, and inflammation and cancer appeared when a defective transforming growth factor β signaling occurred [279]. Ethanol exerts teratogenic effects and is responsible for both fetal alcohol syndrome (FAS) and fetal alcohol spectrum disorders (FASD) [280].…”

Section: Alcohol Cancer Stem Cells Theories and Therapeutic Strategiesmentioning

confidence: 99%

Biochemical Mechanisms Associating Alcohol Use Disorders with Cancers.

Rodríguez

Coveñas

2021

Preprint

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The World Health Organization identifies alcohol as a cause in several neoplasias of the oro-pharynx cavity, esophagus, gastrointestinal tract, larynx, liver, or female breast. This study re-views ethanol's nonoxidative and oxidative metabolism and one-carbon metabolism that en-compasses both redox and transfer reactions that influence crucial cell proliferation machinery. Ethanol favors the uncontrolled production and action of free radicals that interfere with the maintenance of essential cellular functions. We focus on the generation of protein, DNA, and lipid adducts that interfere with the cellular processes related to growth and differentiation. Ethanol's effects on stem cells responsible for building and repairing tissues are reviewed. Cancer stem cells suffer disturbances related to the expression of cell surface markers, enzymes, and transcription factors after ethanol exposure with consequent dysregulation of mechanisms related to cancer metastasis or resistance to treatments. Our analysis aims to underlie and discuss potential targets that show more sensitivity to ethanol's action and identify specific metabolic routes and metabolic realms that may be corrected to recover metabolic homeostasis after pharmacological interven-tion. Specifically, research should pay attention to reestablish metabolic fluxes by fine-tuning the functioning of specific pathways related to one-carbon metabolism and antioxidant processes.

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“…Studies aimed at the identification and analysis of cancer stem cells are limited by the lack of specific cancer stem-cell markers [ 104 ]. Nonetheless, it has been proposed that alcohol may impinge on cancer stem-cell properties [ 105 , 106 ]. The molecular mechanism by which ethanol metabolism contributes to tumorigenesis may be associated to the production of ROS which play a pivotal role in cancer stem-cell maintenance and differentiation [ 105 , 107 ].…”

Section: Effects Of Alcohol On Different Types Of Stem Cellsmentioning

confidence: 99%

Stem cells under the influence of alcohol: effects of ethanol consumption on stem/progenitor cells

Rocco

Baldari

Pani³

et al. 2018

Cell. Mol. Life Sci.

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Stem cells drive embryonic and fetal development. In several adult tissues, they retain the ability to self-renew and differentiate into a variety of specialized cells, thus contributing to tissue homeostasis and repair throughout life span. Alcohol consumption is associated with an increased risk for several diseases and conditions. Growing and developing tissues are particularly vulnerable to alcohol’s influence, suggesting that stem- and progenitor-cell function could be affected. Accordingly, recent studies have revealed the possible relevance of alcohol exposure in impairing stem-cell properties, consequently affecting organ development and injury response in different tissues. Here, we review the main studies describing the effects of alcohol on different types of progenitor/stem cells including neuronal, hepatic, intestinal and adventitial progenitor cells, bone-marrow-derived stromal cell, dental pulp, embryonic and hematopoietic stem cells, and tumor-initiating cells. A better understanding of the nature of the cellular damage induced by chronic and episodic heavy (binge) drinking is critical for the improvement of current therapeutic strategies designed to treat patients suffering from alcohol-related disorders.

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Alcohol, stem cells and cancer

Cited by 10 publications

References 76 publications

CPEB1 mediates hepatocellular carcinoma cancer stemness and chemoresistance

CPEB1 mediates hepatocellular carcinoma cancer stemness and chemoresistance

Biochemical Mechanisms Associating Alcohol Use Disorders with Cancers.

Stem cells under the influence of alcohol: effects of ethanol consumption on stem/progenitor cells

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