Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

The growth of solid tumours requires a blood supply provided by re-modeling of existing blood vessel endothelium (angiogenesis). Little is known about transcription regulators which are specific for the control of tumour angiogenesis. The proto-oncogene LMO2 encodes a LIM domain transcription regulator which controls angiogenesis during mouse embryogenesis where it regulates remodelling of the capillary network into mature vessels. We now show that Lmo2 expression is augmented in tumour endothelium such as mouse thymomas and human lung tumours. The functional significance of this Lmo2 expression was assessed in teratocarcinomas induced in nude mice by subcutaneous implantation of Lmo2-lacZ targeted ES cells. CD31-positive, sprouting endothelium of ES-cell origin occurred in teratocarcinomas from heterozygous Lmo2-lacZ ES cells but none occurred from null Lmo2-lacZ ES cells. Therefore, in this model Lmo2 is an obligatory regulator of neo-vascularization of tumours. These data suggest that LMO2 function may be a drug target in cancer and other conditions characterized by neo-vascularization.

Original publication

DOI

10.1038/sj.onc.1205285

Type

Journal article

Journal

Oncogene

Publication Date

21/02/2002

Volume

21

Pages

1309 - 1315

Keywords

Adaptor Proteins, Signal Transducing, Angiogenesis Inhibitors, Animals, Cell Division, DNA-Binding Proteins, Drug Design, Erythroid Precursor Cells, Humans, Immunohistochemistry, LIM Domain Proteins, Lung Neoplasms, Metalloproteins, Mice, Mice, Nude, Neoplasm Transplantation, Neoplasms, Neovascularization, Pathologic, Proto-Oncogene Proteins, Thymus Neoplasms, Transcription, Genetic, beta-Galactosidase