The shift in ET receptor binding observed in epithelial cancer cells and cancer-associated fibroblasts and endothelial cells may favour ET-1 signals contributing to colorectal cancer growth and neovascularization via ETAR. This may provide the basis for therapeutic use of specific ETAR antagonists as adjuvant treatment of colorectal cancer.
The distribution of endothelin-A- and B- (ET(A), ET(B)) receptor subtypes was compared in colorectal cancer to that in normal colon and their expression in the colorectal cancer cell lines LIM1215. HT29, SKCO1, SKCO17 and LoVo was determined, using gross and high resolution autoradiography and quantified by densitometry. ET(A) and ET(B) binding sites were expressed by all the cell lines. There was significantly (p = 0.008) higher expression of ET(A)-receptors by cancers (205.95 dpm x 1000/mm2) compared normal colon (129.19 dpm x 1000/mm2). However, for ET(B)-receptors, this was reversed, with significantly (p = 0.008) higher expression of ET(B) binding in normal colon (207.00 dpm x 1000/mm2) than in tumours (122.35 dpm x 1000/mm2).
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