Several lines of evidence support an important role of TGF-β in the development of colorectal cancer, although the molecular consequences are largely unknown. Soluble transforming growth factor-β receptor type II (sTβRII) is a target of transforming growth factors-β (TGF-β) that plays an important role in regulation tumorigenesis, angiogenesis and metastasis of cancer. To elucidate whether overexpression of sTβRII could antagonize TGF-β in colon cancer cells, we constructed a plasmid that contains a cDNA encoding human extracellular region of TβRII and transfected this construction into LoVo cells. Surprisingly, in the absence of TGF-β1, the overexpression of sTβRII antagonized TGF-β-induced cell proliferation, invasion, motility and angiogenesis, and decreased expression of VEGF and MMP-9. Also, sTβRII inhibited TGF-β-induced apoptosis and improved the induction of antitumor immunity. Our data indicated that sTβRII attenuated the biological activities of TGF-β, suggesting that sTβRII may have a therapeutic benefit in colorectal cancer.

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