Galectin-1 is silenced by promoter hypermethylation and its re-expression induces apoptosis in human colorectal cancer cells.
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.
Department of Biomedical Sciences, Texas Tech University Health Sciences Center, Amarillo, TX 79106, USA.
Arun
A
Satelli
U Subrahmanyeswara
US
Rao
D017209:Apoptosis / Q000187:drug effects; D002087:Butyrates / Q000494:pharmacology; D020169:Caspases / Q000502:physiology; D002453:Cell Cycle; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D015179:Colorectal Neoplasms / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D019175:DNA Methylation; D037483:Galectin 1 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000502:physiology*; D020868:Gene Silencing; D006801:Humans; D053078:Membrane Potential, Mitochondrial; D011401:Promoter Regions, Genetic
D002087:Butyrates; D037483:Galectin 1; C445499:LGALS1 protein, human; D020169:Caspases