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Assessing the Role of Autophagy in Prostate Cancer

February 16, 2016

Eileen White, PhDResearch from investigators at Rutgers Cancer Institute of New Jersey and the Herbert Irving Comprehensive Cancer Center at Columbia University Medical Center, shows the intracellular process of autophagy plays a role in the development of prostate cancer. Rutgers Cancer Institute Deputy Director Eileen P. White, PhD, distinguished professor of molecular biology and biochemistry in the School of Arts and Sciences at Rutgers, The State University of New Jersey, and Rutgers Cancer Institute Director Robert S. DiPaola, MD, are the co-corresponding authors of the work published in the February 15 edition of Genes & Development (http://www.genesdev.org/cgi/doi/10.1101/gad.274134.115). Dr. White shares more about the work, which also yielded a new laboratory model for studying new approaches to targeting autophagy in prostate cancer:

Q: Why is this topic important to explore?

A: Even though a number of new therapies are now available to treat certain types of prostate cancer that grow despite low levels of testosterone (castrate sensitive and castrate resistant), median survival is only about four years.  While many of these new agents target the hormonal pathway responsible for this growth, these tumors eventually become drug resistant, thus presenting a challenge to clinicians. Understanding the importance of other critical cellular processes that promote aggressive prostate cancer growth may lead to new therapeutic approaches.   

Q: How did you approach this work?

A: Autophagy, a normal cellular process in which intracellular components are recycled leading to sustained cell growth during times of stress, is known to facilitate tumor growth, survival, and malignancy. A role of autophagy in promoting prostate cancer was not known. To assess the importance of autophagy in prostate cancer, we developed a new genetically-engineered mouse model in which we removed the Pten tumor suppressor gene in order to initiate the prostate tumor growth. To assess the role for autophagy, Pten was deleted with and without co-deletion of the autophagy-related-7 (Atg7) gene. We found that the lack of the Atg7 gene delayed tumor progression in both castrate-sensitive and castrate-resistant prostate cancers.

Q: What is the implication of this finding?

A:  This finding suggests that autophagy may promote the development of prostate cancer and that targeting autophagy may have therapeutic benefit. Especially since prostate cancer is slow growing in many cases – perhaps being present for years before becoming aggressive in nature – efforts to understand the underlying cellular survival mechanism of autophagy could lead to methods to better control this disease. Using our new genetically-engineered model, there is an opportunity to test new approaches that are combined with new and known therapies in order to target autophagy inhibition. 


This work was supported in part by the following grants: P30 CA072720, UM1 CA186716, R01 CA163591, R01 CA130893, R01 CA188096; and by the Rutgers Cancer Institute of New Jersey Histopathology Service Core, the Biostatistics Core, and the Rutgers Molecular Imaging Core.

 

Contact: 
Michele Fisher
Phone: 
732-235-9872

 

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