A switch from lysosomal degradation to secretory autophagy initiates osteogenic bone metastasis in prostate cancer

Abstract The identification of both autophagy‐related material degradation and unconventional secretion has paved the way for significant breakthroughs linking autophagy to a plethora of physiological processes and disease conditions. However, the mechanisms that coordinate these two pathways remain...

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Main Authors: Xiaoyu Wei, Mengmeng Liang, Min Deng, Ji Zheng, Fei Luo, Qinyu Ma
Format: Article
Language:English
Published: Wiley 2024-11-01
Series:Journal of Extracellular Vesicles
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Online Access:https://doi.org/10.1002/jev2.70002
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author Xiaoyu Wei
Mengmeng Liang
Min Deng
Ji Zheng
Fei Luo
Qinyu Ma
author_facet Xiaoyu Wei
Mengmeng Liang
Min Deng
Ji Zheng
Fei Luo
Qinyu Ma
author_sort Xiaoyu Wei
collection DOAJ
description Abstract The identification of both autophagy‐related material degradation and unconventional secretion has paved the way for significant breakthroughs linking autophagy to a plethora of physiological processes and disease conditions. However, the mechanisms that coordinate these two pathways remain elusive. Here, we demonstrate that a switch from the lysosomal degradation to a secretory autophagy pathway is governed by protein tyrosine phosphatase 1B (PTP1B, encoded by PTPN1). Dephosphorylation at two tyrosine residues of syntaxin17 (STX17) by PTP1B reduces autophagosome‐lysosome fusion while switching the cells to a secretory autophagy pathway. Both PTP1B overexpression and tumour‐derived extracellular vesicles (EVs) can activate the secretory autophagy pathway in osteoblasts. Moreover, we demonstrate that osteoblastic LC3+ EVs, generated via the secretory autophagy pathway, are the primary contributor to tumour‐associated bone remodelling in prostate cancer. Depletion of tumour‐derived EVs secretion or genetic ablation of osteoblastic PTP1B rescues aberrant bone remodelling and lesions, highlighting the relevance between LC3+ EVs and the formation of bone metastatic niche. Our results reveal the significance of tumour‐regulated PTP1B in the fate decision of autophagosomes, and propose a role ofLC3+ EVs in shaping the bone metastatic niche.
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institution Kabale University
issn 2001-3078
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publishDate 2024-11-01
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spelling doaj-art-7a0056aff96d480e83b4c69ceac564be2024-11-29T11:34:28ZengWileyJournal of Extracellular Vesicles2001-30782024-11-011311n/an/a10.1002/jev2.70002A switch from lysosomal degradation to secretory autophagy initiates osteogenic bone metastasis in prostate cancerXiaoyu Wei0Mengmeng Liang1Min Deng2Ji Zheng3Fei Luo4Qinyu Ma5Department of Orthopedics, Southwest Hospital Third Military Medical University Chongqing ChinaDepartment of Orthopedics, Southwest Hospital Third Military Medical University Chongqing ChinaDepartment of Urology Xinqiao Hospital, Third Military Medical University Chongqing ChinaDepartment of Urology Xinqiao Hospital, Third Military Medical University Chongqing ChinaDepartment of Orthopedics, Southwest Hospital Third Military Medical University Chongqing ChinaDepartment of Orthopedics, Southwest Hospital Third Military Medical University Chongqing ChinaAbstract The identification of both autophagy‐related material degradation and unconventional secretion has paved the way for significant breakthroughs linking autophagy to a plethora of physiological processes and disease conditions. However, the mechanisms that coordinate these two pathways remain elusive. Here, we demonstrate that a switch from the lysosomal degradation to a secretory autophagy pathway is governed by protein tyrosine phosphatase 1B (PTP1B, encoded by PTPN1). Dephosphorylation at two tyrosine residues of syntaxin17 (STX17) by PTP1B reduces autophagosome‐lysosome fusion while switching the cells to a secretory autophagy pathway. Both PTP1B overexpression and tumour‐derived extracellular vesicles (EVs) can activate the secretory autophagy pathway in osteoblasts. Moreover, we demonstrate that osteoblastic LC3+ EVs, generated via the secretory autophagy pathway, are the primary contributor to tumour‐associated bone remodelling in prostate cancer. Depletion of tumour‐derived EVs secretion or genetic ablation of osteoblastic PTP1B rescues aberrant bone remodelling and lesions, highlighting the relevance between LC3+ EVs and the formation of bone metastatic niche. Our results reveal the significance of tumour‐regulated PTP1B in the fate decision of autophagosomes, and propose a role ofLC3+ EVs in shaping the bone metastatic niche.https://doi.org/10.1002/jev2.70002autophagosome‐lysosome fusionbone metastatic nicheextracellular vesiclessecretory autophagytumour‐associated bone remodelling
spellingShingle Xiaoyu Wei
Mengmeng Liang
Min Deng
Ji Zheng
Fei Luo
Qinyu Ma
A switch from lysosomal degradation to secretory autophagy initiates osteogenic bone metastasis in prostate cancer
Journal of Extracellular Vesicles
autophagosome‐lysosome fusion
bone metastatic niche
extracellular vesicles
secretory autophagy
tumour‐associated bone remodelling
title A switch from lysosomal degradation to secretory autophagy initiates osteogenic bone metastasis in prostate cancer
title_full A switch from lysosomal degradation to secretory autophagy initiates osteogenic bone metastasis in prostate cancer
title_fullStr A switch from lysosomal degradation to secretory autophagy initiates osteogenic bone metastasis in prostate cancer
title_full_unstemmed A switch from lysosomal degradation to secretory autophagy initiates osteogenic bone metastasis in prostate cancer
title_short A switch from lysosomal degradation to secretory autophagy initiates osteogenic bone metastasis in prostate cancer
title_sort switch from lysosomal degradation to secretory autophagy initiates osteogenic bone metastasis in prostate cancer
topic autophagosome‐lysosome fusion
bone metastatic niche
extracellular vesicles
secretory autophagy
tumour‐associated bone remodelling
url https://doi.org/10.1002/jev2.70002
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