| 题名 | Acetylation of KLF5 maintains EMT and tumorigenicity to cause chemoresistant bone metastasis in prostate cancer |
| 作者 | Zhang，Baotong1,2  ; Li，Yixiang1,2; Wu，Qiao3; Xie，Lin1,2,4; Barwick，Benjamin1,2; Fu，Changying3,5; Li，Xin6; Wu，Daqing6; Xia，Siyuan1,2; Chen，Jing1,2; Qian，Wei Ping2,7; Yang，Lily2,7; Osunkoya，Adeboye O.2,8; Boise，Lawrence1,2; Vertino，Paula M.2,9; Zhao，Yichao1,2; Li，Menglin1,2; Chen，Hsiao Rong10; Kowalski，Jeanne10; Kucuk，Omer1,2; Zhou，Wei1,2; Dong,Jin-Tang1,2,5
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| 通讯作者 | Dong,Jin-Tang |
| 发表日期 | 2021-03-17
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| DOI | |
| 发表期刊 | |
| ISSN | 2041-1723
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| 卷号 | 12期号:1页码:1714 |
| 摘要 | Advanced prostate cancer (PCa) often develops bone metastasis, for which therapies are very limited and the underlying mechanisms are poorly understood. We report that bone-borne TGF-β induces the acetylation of transcription factor KLF5 in PCa bone metastases, and acetylated KLF5 (Ac-KLF5) causes osteoclastogenesis and bone metastatic lesions by activating CXCR4, which leads to IL-11 secretion, and stimulating SHH/IL-6 paracrine signaling. While essential for maintaining the mesenchymal phenotype and tumorigenicity, Ac-KLF5 also causes resistance to docetaxel in tumors and bone metastases, which is overcome by targeting CXCR4 with FDA-approved plerixafor. Establishing a mechanism for bone metastasis and chemoresistance in PCa, these findings provide a rationale for treating chemoresistant bone metastasis of PCa with inhibitors of Ac-KLF5/CXCR4 signaling. |
| 相关链接 | [Scopus记录] |
| 收录类别 | |
| 语种 | 英语
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| 重要成果 | NI期刊
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| 学校署名 | 通讯
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| 资助项目 | Department of Defense Prostate Cancer Research Program[
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| WOS研究方向 | Science & Technology - Other Topics
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| WOS类目 | Multidisciplinary Sciences
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| WOS记录号 | WOS:000630420900013
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| 出版者 | |
| Scopus记录号 | 2-s2.0-85102688226
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| 来源库 | Scopus
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| 引用统计 |
被引频次[WOS]：76
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| 成果类型 | 期刊论文 |
| 条目标识符 | http://sustech.caswiz.com/handle/2SGJ60CL/222014 |
| 专题 | 南方科技大学医学院_人类细胞生物和遗传学系 南方科技大学医学院 |
| 作者单位 | 1.Department of Hematology and Medical Oncology,Emory University School of Medicine,Atlanta,United States 2.Winship Cancer Institute,Emory University,Atlanta,United States 3.Department of Genetics and Cell Biology,Nankai University College of Life Sciences,Tianjin,China 4.Third Affiliated Hospital of Kunming Medical University,Cancer Hospital of Yunnan Province,Kunming,China 5.Department of Human Cell Biology and Genetics,Southern University of Science and Technology School of Medicine,Shenzhen,China 6.Molecular Oncology and Biomarkers Program,Georgia Cancer Center,Department of Biochemistry and Molecular Biology,Medical College of Georgia,Augusta University,Augusta,United States 7.Department of Surgery,Emory University School of Medicine,Atlanta,United States 8.Department of Pathology and Urology,Emory University School of Medicine,Atlanta,United States 9.Department of Radiation Oncology,Emory University School of Medicine,Atlanta,United States 10.Department of Biostatistics & Bioinformatics,Rollins School of Public Health,Emory University,Atlanta,United States |
| 通讯作者单位 | 人类细胞生物和遗传学系; 南方科技大学医学院 |
| 推荐引用方式 GB/T 7714 |
Zhang，Baotong,Li，Yixiang,Wu，Qiao,et al. Acetylation of KLF5 maintains EMT and tumorigenicity to cause chemoresistant bone metastasis in prostate cancer[J]. Nature Communications,2021,12(1):1714.
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| APA |
Zhang，Baotong.,Li，Yixiang.,Wu，Qiao.,Xie，Lin.,Barwick，Benjamin.,...&Dong,Jin-Tang.(2021).Acetylation of KLF5 maintains EMT and tumorigenicity to cause chemoresistant bone metastasis in prostate cancer.Nature Communications,12(1),1714.
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| MLA |
Zhang，Baotong,et al."Acetylation of KLF5 maintains EMT and tumorigenicity to cause chemoresistant bone metastasis in prostate cancer".Nature Communications 12.1(2021):1714.
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| 条目包含的文件 | ||||||
| 文件名称/大小 | 文献类型 | 版本类型 | 开放类型 | 使用许可 | 操作 | |
| Acetylation of KLF5 （9504KB） | -- | -- | 开放获取 | -- | 浏览 | |
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