HDAC-42 modulates acid-induced gene expression in human SEG-1 esophageal adenocarcinoma cells

The role of acid and bile salts in the pathogenesis of esophageal carcinoma arising from Barrett's metaplasia has been well established. Cell proliferation of Barrett's epithelium in response to pulsatile acid exposure has since been confirmed in vivo using endoscopy specimens. Histone deactylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis to assess the ability of HDAC-42 to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Keywords: acid-pulsed cells pretreated with HDAC inhibitor or vehicle SEG-1 cells were pretreated for 24 hours with vehicle or HDAC-42, pulsed with media or acidified media (pH 3.5; 20 mins at 37C), replenished with media or HDAC-42, and harvested 6 hours later. Global gene expression analysis was conducted using the human genome chip U133 2.0 Plus.