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Autophagy‐Activated Self‐reporting Photosensitizer Promoting Cell Mortality in Cancer Starvation Therapy
Cancer starvation therapy have received continuous attention as an efficient method to fight against wide‐spectrum cancer. However, during cancer starvation therapy, the protective autophagy promotes cancer cells survival, compromising the therapeutic effect. Herein, a novel strategy by combination...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10288242/ https://www.ncbi.nlm.nih.gov/pubmed/37083241 http://dx.doi.org/10.1002/advs.202301295 |
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author | Zhang, Ruoyao Zhang, Chen Chen, Chao Tian, Minggang Chau, Joe H. C. Li, Zhao Yang, Yuanzhan Li, Xiaoqiong Tang, Ben Zhong |
author_facet | Zhang, Ruoyao Zhang, Chen Chen, Chao Tian, Minggang Chau, Joe H. C. Li, Zhao Yang, Yuanzhan Li, Xiaoqiong Tang, Ben Zhong |
author_sort | Zhang, Ruoyao |
collection | PubMed |
description | Cancer starvation therapy have received continuous attention as an efficient method to fight against wide‐spectrum cancer. However, during cancer starvation therapy, the protective autophagy promotes cancer cells survival, compromising the therapeutic effect. Herein, a novel strategy by combination of autophagy‐activated fluorescent photosensitizers (PSs) and cancer starvation therapy to realize the controllable and efficient ablation of tumor is conceived. Two dual‐emissive self‐reporting aggregation‐induced emission luminogens (AIEgens), TPAQ and TPAP, with autophagy‐activated reactive oxygen species (ROS) generation are prepared to fight against the protective autophagy in cancer starvation therapy. When protective autophagy occurs, a portion of TPAQ and TPAP will translocate from lipid droplets to acidic lysosomes with significant redshift in fluorescence emission and enhanced ROS generation ability. The accumulation of ROS induced by TPAQ‐H and TPAP‐H causes lysosomal membrane permeabilization (LMP), which further results in cell apoptosis and promotes cell death. In addition, TPAQ and TPAP can enable the real‐time self‐reporting to cell autophagy and cell death process by observing the change of red‐emissive fluorescence signals. Particularly, the efficient ablation of tumor via the combination of cancer starvation therapy and photodynamic therapy (PDT) induced by TPAQ has been successfully confirmed in 3D tumor spheroid chip, suggesting the validation of this strategy. |
format | Online Article Text |
id | pubmed-10288242 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-102882422023-06-24 Autophagy‐Activated Self‐reporting Photosensitizer Promoting Cell Mortality in Cancer Starvation Therapy Zhang, Ruoyao Zhang, Chen Chen, Chao Tian, Minggang Chau, Joe H. C. Li, Zhao Yang, Yuanzhan Li, Xiaoqiong Tang, Ben Zhong Adv Sci (Weinh) Research Articles Cancer starvation therapy have received continuous attention as an efficient method to fight against wide‐spectrum cancer. However, during cancer starvation therapy, the protective autophagy promotes cancer cells survival, compromising the therapeutic effect. Herein, a novel strategy by combination of autophagy‐activated fluorescent photosensitizers (PSs) and cancer starvation therapy to realize the controllable and efficient ablation of tumor is conceived. Two dual‐emissive self‐reporting aggregation‐induced emission luminogens (AIEgens), TPAQ and TPAP, with autophagy‐activated reactive oxygen species (ROS) generation are prepared to fight against the protective autophagy in cancer starvation therapy. When protective autophagy occurs, a portion of TPAQ and TPAP will translocate from lipid droplets to acidic lysosomes with significant redshift in fluorescence emission and enhanced ROS generation ability. The accumulation of ROS induced by TPAQ‐H and TPAP‐H causes lysosomal membrane permeabilization (LMP), which further results in cell apoptosis and promotes cell death. In addition, TPAQ and TPAP can enable the real‐time self‐reporting to cell autophagy and cell death process by observing the change of red‐emissive fluorescence signals. Particularly, the efficient ablation of tumor via the combination of cancer starvation therapy and photodynamic therapy (PDT) induced by TPAQ has been successfully confirmed in 3D tumor spheroid chip, suggesting the validation of this strategy. John Wiley and Sons Inc. 2023-04-21 /pmc/articles/PMC10288242/ /pubmed/37083241 http://dx.doi.org/10.1002/advs.202301295 Text en © 2023 The Authors. Advanced Science published by Wiley‐VCH GmbH https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Zhang, Ruoyao Zhang, Chen Chen, Chao Tian, Minggang Chau, Joe H. C. Li, Zhao Yang, Yuanzhan Li, Xiaoqiong Tang, Ben Zhong Autophagy‐Activated Self‐reporting Photosensitizer Promoting Cell Mortality in Cancer Starvation Therapy |
title | Autophagy‐Activated Self‐reporting Photosensitizer Promoting Cell Mortality in Cancer Starvation Therapy |
title_full | Autophagy‐Activated Self‐reporting Photosensitizer Promoting Cell Mortality in Cancer Starvation Therapy |
title_fullStr | Autophagy‐Activated Self‐reporting Photosensitizer Promoting Cell Mortality in Cancer Starvation Therapy |
title_full_unstemmed | Autophagy‐Activated Self‐reporting Photosensitizer Promoting Cell Mortality in Cancer Starvation Therapy |
title_short | Autophagy‐Activated Self‐reporting Photosensitizer Promoting Cell Mortality in Cancer Starvation Therapy |
title_sort | autophagy‐activated self‐reporting photosensitizer promoting cell mortality in cancer starvation therapy |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10288242/ https://www.ncbi.nlm.nih.gov/pubmed/37083241 http://dx.doi.org/10.1002/advs.202301295 |
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