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

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

Author information

1
Department of Biomedical Sciences, Texas Tech University Health Sciences Center, Amarillo, TX 79106, USA.

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.

PMID:
21122983
PMCID:
PMC3023883
DOI:
10.1016/j.canlet.2010.10.027
[Indexed for MEDLINE]
Free PMC Article

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