Abstract
Several lines of evidence support an important role of TGF-beta in the development of colorectal cancer, although the molecular consequences are largely unknown. Soluble transforming growth factor-beta receptor type II (sTbetaRII) is a target of transforming growth factors-beta (TGF-beta) that plays an important role in regulation tumorigenesis, angiogenesis and metastasis of cancer. To elucidate whether overexpression of sTbetaRII could antagonize TGF-beta in colon cancer cells, we constructed a plasmid that contains a cDNA encoding human extracellular region of TbetaRII and transfected this construction into LoVo cells. Surprisingly, in the absence of TGF-beta1, the overexpression of sTbetaRII antagonized TGF-beta-induced cell proliferation, invasion, motility and angiogenesis, and decreased expression of VEGF and MMP-9. Also, sTbetaRII inhibited TGF-beta-induced apoptosis and improved the induction of antitumor immunity. Our data indicated that sTbetaRII attenuated the biological activities of TGF-beta, suggesting that sTbetaRII may have a therapeutic benefit in colorectal cancer.
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