Blocking PGE2-induced tumour repopulation abrogates bladder cancer chemoresistance

Antonina V. Kurtova, Jing Xiao, Qianxing Mo, Senthil Pazhanisamy, Ross Krasnow, Seth P. Lerner, Fengju Chen, Terrence T. Roh, Erica Lay, Philip Levy Ho and Keith Syson Chan ()
Additional contact information
Antonina V. Kurtova: Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
Jing Xiao: Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
Qianxing Mo: Dan L Duncan Cancer Center and Center for Cell Gene & Therapy, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
Senthil Pazhanisamy: Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
Ross Krasnow: Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
Seth P. Lerner: Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
Fengju Chen: Dan L Duncan Cancer Center and Center for Cell Gene & Therapy, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
Terrence T. Roh: Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
Erica Lay: Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
Philip Levy Ho: Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
Keith Syson Chan: Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA

Nature, 2015, vol. 517, issue 7533, 209-213

Abstract: Using human bladder cancer xenograft models, a new mechanism involving an active proliferative response of cancer stem cells to chemotherapy-induced damage is shown, driven by prostaglandin E2 (PGE2) release in a manner similar to PGE2-induced wound repair; pharmacological inhibition of the PGE2/COX2 axis by celecoxib attenuates chemoresistance, suggesting a possible adjunctive therapy for bladder carcinomas.

Date: 2015
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DOI: 10.1038/nature14034

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