Could modulation of SPDEF activity lower risk for metastatic prostate cancer?


According to an article just published in the Journal of Biological Chemistry, the authors have identified a biological molecule known as the SAM pointed domain ETS transcription factor or SPDEF controls the expression of E-cadherin — a protein that is known to be very important to the process of prostate cancer metastasis.

Pal et al. report that SPDEF acts as a switch that can turn on and off the expression of E-cadherin. In a blog post from the University of Colorado Cancer Center, Prof. Hari Koul, the senior author of the paper, is quoted as follows:

When E-cadherin is lost, cells … can detach from their surrounding tissues, move effortlessly through the circulatory system, grow and attach at new sites. In prostate tumors that had lost E-cadherin, we put in SPDEF and the tumors once again expressed E-cadherin.

In other words, if we can modify the activity of SPDEF to regulate the expression of E-cadherin, we may have a completely new way to limit the risk for prostate cancer metastasis.

Now, as we point out regularly, the translation of this type of basic research into clinically effective types of treatment is often challenging, and it can’t be assumed that such translational research efforts will necessarily lead to a drug or drugs that can modify the activity of SPDEF and the expression of E-cadherin. However, these findings certainly open a new doorway that could be critical to development of a new class of drugs with utility in the management of progressive prostate cancer.

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