Fox Chase researchers uncover one force behind the MYC oncogene in ma...( Philadelphia (July 27 2009) DLX5 a ...)

Philadelphia (July 27, 2009) DLX5, a gene crucial for embryonic development, promotes cancer by activating the expression of the known oncogene, MYC, according to researchers from Fox Chase Cancer Center. Since the DLX5 gene is inactive in normal adults, it may be an ideal target for future anti-cancer drugs, they reason. Their findings are published in the July 31 edition of the Journal of Biological Chemistry, available online now.

Previously the researchers found that a chromosomal inversion a genetic misalignment, where part of the chromosome containing the DLX5 gene gets flipped around during cell division cooperates with another known oncogene, AKT2, to drive cancer in mice. In the current paper, the researchers discover that DLX5 binds to and actively promotes the activity of a gene known as MYC, which evidence has demonstrated is a potent factor in numerous cancers, including lymphoma, lung and pancreatic cancer. Their studies were performed in mouse cancer models and in human cell cultures.

"While MYC has a definite role in cancer, MYC also has an important place in the normal functioning of cells, so it may be difficult to target without killing healthy cells," says Joseph Testa, PhD, a Fox Chase professor and co-author of the study. "DLX5, however, is not generally active in healthy adult cells, so it represents a much more 'druggable' target for cancer inhibition."

According to Testa, DLX5 is a member of the homeobox family of genes, which direct the timing of events in the physical development of a growing fetus, such as when to sprout a limb, for example. In adults, such genes are almost entirely inactive.

After their previous studies demonstrated that expression of the protein encoded by the DLX5 gene correlated with that of the MYC gene, Testa and Jinfei Xu, PhD, a research associate in the laboratory, used a luciferase assay developed from the luciferase enzyme fireflies use to make light to see e
'/>"/>