Convergent evolution of p38/MAPK activation in hormone resistant prostate cancer mediates pro-survival, immune evasive, and metastatic phenotypes
Ware, K. E.; Gupta, S.; Eng, J.; Kemeny, G.; Puviindran, B. J.; Foo, W.-C.; Crawford, L. A.; Almquist, R. G.; Runyambo, D.; Thomas, B. C.; Sheth, M. U.; Agarwal, A.; Pierobon, M.; Petricoin, E. F.; Corcoran, D. L.; Freedman, J.; Patierno, S. R.; Zhang, T.; Gregory, S.; Sychev, Z.; Drake, J. M.; Armstrong, A. J.; Somarelli, J.
Show abstract
Adaptation of cancer cells to targeted therapy follows ecological paradigms observed in natural populations that encounter resource depletion and changing environments, including activation of pro-survival mechanisms, migration to new locations, and escape of predation. We identified the p38 MAPK pathway as a common molecular driver of these three responses during the adaptation to hormone therapy resistance in prostate cancer. The p38 pathway is activated in therapy-resistant cells and mechanistically drives these three convergent responses through sustained AR activity, enhanced invasion and metastasis, and immune evasion. Targeting p38 signaling may represent a new therapeutic strategy to treat men with metastatic, hormone therapy-resistant prostate cancer.
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