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Fox Chase researchers uncover one force behind the MYC oncogene in many cancers
Date:7/28/2009

xactly where DLX5 protein binds to the promoter region of the MYC gene. They found that there were two sites where DLX5 could bind to the MYC promoter, which is a section of DNA where certain proteins known as transcription factors attach in order to recruit the cellular machinery used to transcribe genes into messenger RNA and then proteins. Studies in both cells and a mouse model for cancer showed that they could promote the expression of MYC by transfecting cells with DNA strands containing DLX5.

Too much DLX5, they found, led to too much MYC. When they knocked out expression of DLX5 in lung cancer cells, it resulted in decreased expression of MYC and reduced cell proliferation. By adding an overabundance of MYC, they found they could turn those cells cancerous again.

From this, Testa and Xu were able to gain a broader understanding of how cancers involving AKT2, DLX5 and MYC might develop. A mutation in AKT2 may act as a "first hit" that makes the inversion on mouse chromosome 6, which contains the DLX5 gene, more likely. When the inversion happens, the cell begins producing the DLX5 protein, a multipurpose transcription factor that normally has a very limited role in adult cells. One of the targets of DLX5 is the MYC gene itself, causing the cells to produce many copies of the MYC oncoprotein.

Normally MYC regulates many functions within the cell, including cell division. With an overabundance of MYC, the cell may reproduce out of control, accumulating in each generation the further genetic damage that is the hallmark of cancer cells.


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Contact: Greg Lester
gregory.lester@fccc.edu
215-728-2753
Fox Chase Cancer Center
Source:Eurekalert

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