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Updated: Jun 27, 2026

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All-trans retinoic acid induces XAF1 expression through an interferon regulatory factor-1 element in colon cancer

Jide Wang1, Ying Peng, Yun Wei Sun

  • 1Institute for Digestive Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, People's Republic of China.

Gastroenterology
|March 15, 2006
PubMed
Abstract

Insights

All-trans retinoic acid (ATRA) upregulates X-linked inhibitor of apoptosis protein (XIAP)-associated factor 1 (XAF1) via IRF-1. XAF1 mediates ATRA

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • X-linked inhibitor of apoptosis protein (XIAP)-associated factor 1 (XAF1) is a novel tumor suppressor and interferon (IFN)-stimulated gene.
  • All-trans retinoic acid (ATRA) exhibits antiproliferative effects on tumor cells by upregulating IFN regulatory factor 1 (IRF-1) and downstream IFN-stimulated genes.

Purpose of the Study:

  • To investigate the effect of ATRA on XAF1 expression and its mechanism.
  • To determine the role of XAF1 in ATRA-induced growth inhibition in colon cancer.

Main Methods:

  • Gene expression analysis using reverse-transcription polymerase chain reaction and immunoblotting.
  • Luciferase reporter assay to assess XAF1 promoter activity.
  • Electrophoretic mobility shift assay and chromatin immunoprecipitation to evaluate IRF-1 binding element activity.
  • In vitro and in vivo assessment of cell growth in nude mice xenografts.

Main Results:

  • IFN-alfa dose-dependently stimulates XAF1 promoter activity in colon cancer cells.
  • An IRF-1 binding element (IRF-E-XAF1) located in the promoter region is crucial for XAF1 activity.
  • ATRA induces XAF1 expression in vitro and in vivo through interaction with IRF-E-XAF1, enhancing susceptibility to growth suppression.

Conclusions:

  • XAF1 plays a role in ATRA-induced growth suppression in colon cancer.
  • This effect is mediated by IRF-1-dependent transcriptional regulation of XAF1.

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