Prostate cancer is one of the most frequent cancers among men. It is estimated that 80% of men who reach age 80 will be diagnosed with the disease. Now, a study from researchers at Wistar Institute researchers shows that the TRAP1 protein drives prostate cancer.
A growing body of evidence shows that tumors regulate genes and proteins that are involved in energy production so that they can stay alive. Mitochondria are an important organelle that is responsible for energy production. Mitochondria of tumor cells contain higher levels of a molecular chaperone celled HSP90. HSP90 aids the folding of newly synthesized proteins, enabling them to be folded properly. Another chaperone protein called TRAP1 is structurally similar to HSP90, and it functions to regulate energy production.
Wistar researchers previously found that TRAP1 seems to be implicated in tumor growth. They deleted the TRAP1 protein from mice to see how it may affects disease development. The TRAP1-knockout mice lived longer and had less age-related diseases, indicating that TRAP1 has a role in disease. However, the role of the protein in prostate cancer development remained to be answered.
For this study, Wistar researchers created mice that overexpressed TRAP1 and lost one copy of the PTEN gene (Pten+/-). Gene PTEN is a tumor suppressor that is mutated in many cancers at high frequency. The loss of PTEN is found in approximately 40% of all prostate cancer cases, and PTEN mutations are associated with drug resistance.
The Pten+/- mice that had increased TRAP1 developed aggressive, early-onset invasive prostate cancer. The results indicated that TRAP1 might cause prostate cancer to become more invasive. Protein TRAP1 could be a therapeutic target for prostate cancer, according to lead researcher Dario C. Altieri.