Acetylation of KLF5 maintains EMT and tumorigenicity to cause chemoresistant bone metastasis in prostate cancer

Acetylation of KLF5 maintains EMT and tumorigenicity to cause chemoresistant bone metastasis in prostate cancer

The therapies for bone metastatic prostate cancer are limited and the underlying mechanisms are unclear. Here, the authors show that bone derived TGF-β induces acetylation of KLF5 (Ac-KLF5), and Ac-KLF5 promotes prostate cancer bone metastasis and resistance to docetaxel by upregulating CXCR4.

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Detalles Bibliográficos
Autores principales: Baotong Zhang, Yixiang Li, Qiao Wu, Lin Xie, Benjamin Barwick, Changying Fu, Xin Li, Daqing Wu, Siyuan Xia, Jing Chen, Wei Ping Qian, Lily Yang, Adeboye O. Osunkoya, Lawrence Boise, Paula M. Vertino, Yichao Zhao, Menglin Li, Hsiao-Rong Chen, Jeanne Kowalski, Omer Kucuk, Wei Zhou, Jin-Tang Dong
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
Materias:
Science
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Acceso en línea:https://doaj.org/article/4767d9e2f20b432ab88e90cb4777af44
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Descripción
Sumario:The therapies for bone metastatic prostate cancer are limited and the underlying mechanisms are unclear. Here, the authors show that bone derived TGF-β induces acetylation of KLF5 (Ac-KLF5), and Ac-KLF5 promotes prostate cancer bone metastasis and resistance to docetaxel by upregulating CXCR4.

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