Abrogation of alcohol dehydrogenase-1B expression by CD90+ stromal cells supports tumor-promoting inflammation in colorectal cancer

Date 29 June 2016
Event ESMO World Congress on Gastrointestinal Cancer 2016
Session ESMO World Congress on Gastrointestinal Cancer 2016 - Abstracts book
Presenter R. Villéger
Citation Annals of Oncology (2016) 27 (2): 1-85. 10.1093/annonc/mdw199
Authors R. Villéger1, E. Beswick2, P. Johnson1, S. Qiu1, D. Powell1, I. Pinchuk1
  • 1University of Texas Medical Branch, Galveston, Texas, USA, /
  • 2University of New Mexico, Albuquerque, New Mexico, USA, /

Abstract

Members of the alcohol dehydrogenase (ADH) enzyme family metabolize a wide variety of substrates, including C2-C4 alcohols and alcohol form of Vitamin A, retinol (RO). ADH1B, a major isoform expressed in normal colon, is implicated in the conversion of vitamin A to retinoic acid (RA), an oxidized form of RO known to be a potent anti-inflammatory molecule. We and others have recently reported a dramatic decrease in ADH1B mRNA expression in colorectal cancer (CRC). However, the pathophysiological role of downregulation of ADH1B in cancer development and progression remains unknown. Thus, in this work, we determined the cell-type specific source associated with ADH1B decrease and hypothesize that a suppression of RO-metabolizing enzyme, ADH1B, promotes tumor-associated inflammatory responses in CRC.