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Cancer BiologybioRxiv
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Convergent evolution of p38/MAPK activation in hormone resistant prostate cancer mediates pro-survival, immune evasive, and metastatic phenotypes

K. E. Ware, S. Gupta, J. Eng, G. Kemeny, B. J. Puviindran, W.-C. Foo, L. A. Crawford, R. G. Almquist, D. Runyambo, B. C. Thomas, M. U. Sheth, A. Agarwal, M. Pierobon, E. F. Petricoin, D. L. Corcoran, J. Freedman, S. R. Patierno, T. Zhang, S. Gregory, Z. Sychev, J. M. Drake, A. J. Armstrong, J. Somarelli

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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