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. 2017 May 15:612:25-28.
doi: 10.1016/j.gene.2016.09.046. Epub 2016 Sep 30.

Alcohol-associated cancer and deregulation of Pol III genes

Ganggang Shi  1 , Shuping Zhong  2
Affiliations

Alcohol-associated cancer and deregulation of Pol III genes

Ganggang Shi et al. Gene. .

Abstract

Emerging evidence indicates that alcohol intake is associated with human cancers in different organs. However, the molecular mechanism of alcohol-associated human cancers remains to be elucidated. Here, this paper aimed to clarify a novel mechanism of alcohol-promoted cell transformation and tumor development. Alcohol induces JNK1 activation and increases cellular levels of c-Jun to upregulate Brf1 expression and Pol III gene transcription, leading to an enhancement of rates of cell transformation and tumor formation.

Keywords: Alcohol; Breast cancer; Brf1; HCC; Pol III genes.

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Conflict of interest statement

Conflict of interest

The authors declare no conflict of interest.

Figures

Fig. 1
Fig. 1. Schematic illustration of a common mechanism of alcohol-associated cancers
Alcohol increases Brf1 expression through JNK1 and c-Jun pathway, which in turn upregulates Pol III gene transcription to promote cell transformation and tumor development caused by alcohol.
See this image and copyright information in PMC

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