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Autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer
Prostate cancer is a common malignant tumor, which can spread to multiple organs in the body. Metastatic disease is the dominant reason of death for patients with prostate cancer. Prostate cancer usually transfers to bone. Bone metastases are related to pathologic fracture, pain, and reduced surviva...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8492756/ https://www.ncbi.nlm.nih.gov/pubmed/34611139 http://dx.doi.org/10.1038/s41419-021-04181-x |
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author | Wang, YouZhi Wu, Ning Jiang, Ning |
author_facet | Wang, YouZhi Wu, Ning Jiang, Ning |
author_sort | Wang, YouZhi |
collection | PubMed |
description | Prostate cancer is a common malignant tumor, which can spread to multiple organs in the body. Metastatic disease is the dominant reason of death for patients with prostate cancer. Prostate cancer usually transfers to bone. Bone metastases are related to pathologic fracture, pain, and reduced survival. There are many known targets for prostate cancer treatment, including androgen receptor (AR) axis, but drug resistance and metastasis eventually develop in advanced disease, suggesting the necessity to better understand the resistance mechanisms and consider multi-target medical treatment. Because of the limitations of approved treatments, further research into other potential targets is necessary. Metastasis is an important marker of cancer development, involving numerous factors, such as AKT, EMT, ECM, tumor angiogenesis, the development of inflammatory tumor microenvironment, and defect in programmed cell death. In tumor metastasis, programmed cell death (autophagy, apoptosis, and necroptosis) plays a key role. Malignant cancer cells have to overcome the different forms of cell death to transfer. The article sums up the recent studies on the mechanism of bone metastasis involving key regulatory factors such as macrophages and AKT and further discusses as to how regulating autophagy is crucial in relieving prostate cancer bone metastasis. |
format | Online Article Text |
id | pubmed-8492756 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-84927562021-10-07 Autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer Wang, YouZhi Wu, Ning Jiang, Ning Cell Death Dis Review Article Prostate cancer is a common malignant tumor, which can spread to multiple organs in the body. Metastatic disease is the dominant reason of death for patients with prostate cancer. Prostate cancer usually transfers to bone. Bone metastases are related to pathologic fracture, pain, and reduced survival. There are many known targets for prostate cancer treatment, including androgen receptor (AR) axis, but drug resistance and metastasis eventually develop in advanced disease, suggesting the necessity to better understand the resistance mechanisms and consider multi-target medical treatment. Because of the limitations of approved treatments, further research into other potential targets is necessary. Metastasis is an important marker of cancer development, involving numerous factors, such as AKT, EMT, ECM, tumor angiogenesis, the development of inflammatory tumor microenvironment, and defect in programmed cell death. In tumor metastasis, programmed cell death (autophagy, apoptosis, and necroptosis) plays a key role. Malignant cancer cells have to overcome the different forms of cell death to transfer. The article sums up the recent studies on the mechanism of bone metastasis involving key regulatory factors such as macrophages and AKT and further discusses as to how regulating autophagy is crucial in relieving prostate cancer bone metastasis. Nature Publishing Group UK 2021-10-05 /pmc/articles/PMC8492756/ /pubmed/34611139 http://dx.doi.org/10.1038/s41419-021-04181-x Text en © The Author(s) 2021, corrected publication 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Review Article Wang, YouZhi Wu, Ning Jiang, Ning Autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer |
title | Autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer |
title_full | Autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer |
title_fullStr | Autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer |
title_full_unstemmed | Autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer |
title_short | Autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer |
title_sort | autophagy provides a conceptual therapeutic framework for bone metastasis from prostate cancer |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8492756/ https://www.ncbi.nlm.nih.gov/pubmed/34611139 http://dx.doi.org/10.1038/s41419-021-04181-x |
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