Galectin-1 is silenced by promoter hypermethylation and its re-expression induces apoptosis in human colorectal cancer cells

Cancer Lett. 2011 Feb 1;301(1):38-46. doi: 10.1016/j.canlet.2010.10.027. Epub 2010 Nov 30.

Abstract

Galectin-1 (gal-1) is an important molecule secreted by many tumors, which induces apoptosis in activated T-cells and promotes tumor angiogenesis, both of which phenomena facilitate successful establishment of tumor in the body. However, little is known about the function of intracellular gal-1 or its transcriptional regulation in colorectal cancer (CRC). Here, we demonstrate that gal-1 expression is epigenetically regulated in CRC through promoter hypermethylation. Intracellular gal-1 induces cell cycle arrest and apoptosis in CRC cells with concomitant down-regulation of Wnt and NF-κB signaling pathways. Together, these data suggested that gal-1 silencing imparts CRC with the ability to proliferate and escape apoptosis.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Apoptosis* / drug effects
  • Butyrates / pharmacology
  • Caspases / physiology
  • Cell Cycle
  • Cell Line, Tumor
  • Cell Proliferation
  • Colorectal Neoplasms / etiology*
  • Colorectal Neoplasms / genetics
  • Colorectal Neoplasms / pathology
  • DNA Methylation*
  • Galectin 1 / antagonists & inhibitors
  • Galectin 1 / genetics
  • Galectin 1 / physiology*
  • Gene Silencing*
  • Humans
  • Membrane Potential, Mitochondrial
  • Promoter Regions, Genetic*

Substances

  • Butyrates
  • Galectin 1
  • LGALS1 protein, human
  • Caspases