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Scientists find key to gene that promotes cancer metastasis
Date:4/12/2010

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This cancer-promoting pathway is the second way Skp2 fuels cancer growth, Lin said. Skp2 has been shown to work through a separate E3 ligase pathway to destroy tumor-suppressing proteins, causing heightened cellular proliferation and the transition from normal cell to tumor.

"Skp2's E3 ligase activity is required for tumorigenesis, but not involved at all in metastasis," Lin said. Lin and colleagues also previously found that Skp2 blocks cellular senescence a halt in cell division in cancer cells.

The research team then found that Skp2 recruits two other proteins, p300 and Miz1, to join Myc and form the complex that transcribes RhoA.

Experiments in a mouse model of breast cancer metastasis to the lung showed that deficiency of either Myc, Skp2 or Miz1 restricted metastasis, while overexpression of each of the three proteins increased cell migration and invasion. Skp2 knockdown, for example, resulted in no metastatic nodules in the lung, compared with an average of 40 nodules when Skp2 was expressed.

Directly knocking down RhoA expression produced the same effect as blocking the Myc-Skp2-Miz1 complex. Knocking down expression of p300 resulted in decreased expression of RhoA.

In the analysis of prostate cancer tumors, expression of RhoA, Myc, Skp2 and Miz1 were significantly correlated with metastasis. Expression of the RhoA and the Myc-Skp2-Miz1 complex also were highly correlated.

Lin and colleagues note that Miz1 is thought to be a tumor-suppressor that contends with the oncogene Myc to regulate genes. In this case, the tumor-suppressor cooperates with the oncogene to launch RhoA and promote metastasis.

"Right now, there are no small-molecule agents to inhibit any of these targets," Lin said. "One future direction of research will be to find ways to target the entire transcription complex or its individual components."


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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert  

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