Several laboratories have studied "in vitro" tumor cell angiogenesis using antisense constructs to the perlecan message. The full-length reverse complement cDNA, driven by a strong promoter, is transfected into various cell types to completely eliminate perlecan expression. Antisense in colon carcinoma cells blocks perlecan translation, leading to decreased tumor growth and angiogenesis. A similar in vitro decrease in proliferation occurred in NIH 3T3 cells and a human melanoma cell line expressing antisense perlecan mRNA. Findings in vitro with Kaposi's sarcoma cell lines showed that loss of perlecan via transfection with an antisense construct led to decreased proliferation and migration of this highly metastatic cell type. These results are in contrast to "in vivo" results with the same Kaposi Sarcoma lines, which show that decreased perlecan leads to increased angiogenesis, which facilitates migration and thus is associated with increase in tumor grade. Antisense knockdown of perlecan in fibrosarcoma cell lines led to increased growth and migration both in vitro and in vivo. These findings of greater tumorigenesis in vivo are supported by data showing that the C-terminus of the perlecan protein acts as an endostatic module now known as endorepellin.