cells can regulate gene expression in growing vessels and the surrounding stroma during tumor neovascularization. T-cadherin expression was found to be altered in tumor vessels: in Lewis carcinoma lung metastasis the expression of T-cadherin was upregulated in blood vessels penetrating the tumor, while T-cadherin was not detected in the surrounding tumor tissue. In tumor neovascularization of hepatocellular carcinoma (HCC) T-cadherin is upregulated in intratumoral capillary endothelial cells, whereas in surrounding tumor tissue as well as in normal liver no T-cadherin could be detected. The increase in T-cadherin expression in endothelial cell in HCC was shown to correlate with tumors progression. Presumably, T-cadherin could play a navigating role in the growing tumor vessels, which in the absence of contact inhibition from the stromal cells, grow into the surrounding tumor tissue. Guiding molecules in vascular and nervous systems T-cadherin was originally cloned from chick embryo brain, where it was implicated as a negative guiding cue for motor axon projecting through the somitic sclerotome and presumably for migrating neural crest cells . As a substrate or in soluble form, T-cadherin inhibits neurite outgrowth by motor neurons in vitro supporting the assumption that T-cadherin acts as a negative guiding molecule in the developing nervous system. Considering that the maximal expression of T-cadherin has been observed in nervous and cardiovascular systems, it is likely that T-cadherin is involved in guiding the growing vessel as well. The mechanism of T-cadherin mediated negative guidance in nervous system involves homophilic interaction and contact inhibition; in vascular system it is supposed that T-cadherin expressing blood vessels would avoid T-cadherin expressing tissues. References Bibliography Further reading External links