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.

Bibliographic Details
Main Authors: 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
Format: Article
Language:English
Published: Nature Publishing Group 2021-03-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-021-21976-w
Description
Summary: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.
ISSN:2041-1723