EZH2 engages TGFβ signaling to promote breast cancer bone metastasis via integrin β1-FAK activation

Breast cancer cells are known to metastasize to the bone but why the cells should migrate and metastasize to this particular organ is not clearly understood. Here, the authors show that EZH2 activates an integrin B1 and FAK signaling pathway in breast cancer cells, which activates TGFB signaling to...

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Main Authors: Lin Zhang, Jingkun Qu, Yutao Qi, Yimin Duan, Yu-Wen Huang, Zhifen Zhou, Ping Li, Jun Yao, Beibei Huang, Shuxing Zhang, Dihua Yu
Format: Article
Language:English
Published: Nature Portfolio 2022-05-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-022-30105-0
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author Lin Zhang
Jingkun Qu
Yutao Qi
Yimin Duan
Yu-Wen Huang
Zhifen Zhou
Ping Li
Jun Yao
Beibei Huang
Shuxing Zhang
Dihua Yu
author_facet Lin Zhang
Jingkun Qu
Yutao Qi
Yimin Duan
Yu-Wen Huang
Zhifen Zhou
Ping Li
Jun Yao
Beibei Huang
Shuxing Zhang
Dihua Yu
author_sort Lin Zhang
collection DOAJ
description Breast cancer cells are known to metastasize to the bone but why the cells should migrate and metastasize to this particular organ is not clearly understood. Here, the authors show that EZH2 activates an integrin B1 and FAK signaling pathway in breast cancer cells, which activates TGFB signaling to drive metastasis in the bone.
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spelling doaj.art-05aa232c6afd450daf8510c54d82f59b2022-12-22T03:34:10ZengNature PortfolioNature Communications2041-17232022-05-0113111610.1038/s41467-022-30105-0EZH2 engages TGFβ signaling to promote breast cancer bone metastasis via integrin β1-FAK activationLin Zhang0Jingkun Qu1Yutao Qi2Yimin Duan3Yu-Wen Huang4Zhifen Zhou5Ping Li6Jun Yao7Beibei Huang8Shuxing Zhang9Dihua Yu10Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterIntelligent Molecular Discovery Laboratory, Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer CenterMD Anderson Cancer Center UTHealth Graduate School of Biomedical SciencesDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer CenterBreast cancer cells are known to metastasize to the bone but why the cells should migrate and metastasize to this particular organ is not clearly understood. Here, the authors show that EZH2 activates an integrin B1 and FAK signaling pathway in breast cancer cells, which activates TGFB signaling to drive metastasis in the bone.https://doi.org/10.1038/s41467-022-30105-0
spellingShingle Lin Zhang
Jingkun Qu
Yutao Qi
Yimin Duan
Yu-Wen Huang
Zhifen Zhou
Ping Li
Jun Yao
Beibei Huang
Shuxing Zhang
Dihua Yu
EZH2 engages TGFβ signaling to promote breast cancer bone metastasis via integrin β1-FAK activation
Nature Communications
title EZH2 engages TGFβ signaling to promote breast cancer bone metastasis via integrin β1-FAK activation
title_full EZH2 engages TGFβ signaling to promote breast cancer bone metastasis via integrin β1-FAK activation
title_fullStr EZH2 engages TGFβ signaling to promote breast cancer bone metastasis via integrin β1-FAK activation
title_full_unstemmed EZH2 engages TGFβ signaling to promote breast cancer bone metastasis via integrin β1-FAK activation
title_short EZH2 engages TGFβ signaling to promote breast cancer bone metastasis via integrin β1-FAK activation
title_sort ezh2 engages tgfβ signaling to promote breast cancer bone metastasis via integrin β1 fak activation
url https://doi.org/10.1038/s41467-022-30105-0
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