Carrier Free Photodynamic Synergists for Oxidative Damage Amplified Tumor Therapy
Tumor cells adapt to excessive oxidative stress by actuating reactive oxygen species (ROS)‐defensing system, leading to a resistance to oxidation therapy. In this work, self‐delivery photodynamic synergists (designated as PhotoSyn) are developed for oxidative damage amplified tumor therapy. Specific...
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| Published in | Small (Weinheim an der Bergstrasse, Germany) Vol. 17; no. 40; pp. e2102470 - n/a |
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| Main Authors | , , , , , , , , , |
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| Language | English |
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01.10.2021
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| Abstract | Tumor cells adapt to excessive oxidative stress by actuating reactive oxygen species (ROS)‐defensing system, leading to a resistance to oxidation therapy. In this work, self‐delivery photodynamic synergists (designated as PhotoSyn) are developed for oxidative damage amplified tumor therapy. Specifically, PhotoSyn are fabricated by the self‐assembly of chlorine e6 (Ce6) and TH588 through π–π stacking and hydrophobic interactions. Without additional carriers, nanoscale PhotoSyn possess an extremely high drug loading rate (up to 100%) and they are found to be fairly stable in aqueous phase with a uniform size distribution. Intravenously injected PhotoSyn prefer to accumulate at tumor sites for effective cellular uptake. More importantly, TH588‐mediated MTH1 inhibition could destroy the ROS‐defensing system of tumor cells by preventing the elimination of 8‐oxo‐2′‐deoxyguanosine triphosphate (8‐oxo‐dG), thereby exacerbating the oxidative DNA damage induced by the photodynamic therapy (PDT) of Ce6 under light irradiation. As a consequence, PhotoSyn exhibit enhanced photo toxicity and a significant antitumor effect. This amplified oxidative damage strategy improves the PDT efficiency with a reduced side effect by increasing the lethality of ROS without generating superabundant ROS, which would provide a new insight for developing self‐delivery nanoplatforms in photodynamic tumor therapy in clinic.
Carrier free photodynamic synergists are developed for oxidative damage amplified tumor therapy by destroying the reactive oxygen species (ROS)‐defensing system without generating excessive ROS, which shed light on the development of self‐delivery nanoplatforms for efficient photodynamic therapy by utilizing the limited oxygen in hypoxic tumors. |
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| AbstractList | Tumor cells adapt to excessive oxidative stress by actuating reactive oxygen species (ROS)‐defensing system, leading to a resistance to oxidation therapy. In this work, self‐delivery photodynamic synergists (designated as PhotoSyn) are developed for oxidative damage amplified tumor therapy. Specifically, PhotoSyn are fabricated by the self‐assembly of chlorine e6 (Ce6) and TH588 through π–π stacking and hydrophobic interactions. Without additional carriers, nanoscale PhotoSyn possess an extremely high drug loading rate (up to 100%) and they are found to be fairly stable in aqueous phase with a uniform size distribution. Intravenously injected PhotoSyn prefer to accumulate at tumor sites for effective cellular uptake. More importantly, TH588‐mediated MTH1 inhibition could destroy the ROS‐defensing system of tumor cells by preventing the elimination of 8‐oxo‐2′‐deoxyguanosine triphosphate (8‐oxo‐dG), thereby exacerbating the oxidative DNA damage induced by the photodynamic therapy (PDT) of Ce6 under light irradiation. As a consequence, PhotoSyn exhibit enhanced photo toxicity and a significant antitumor effect. This amplified oxidative damage strategy improves the PDT efficiency with a reduced side effect by increasing the lethality of ROS without generating superabundant ROS, which would provide a new insight for developing self‐delivery nanoplatforms in photodynamic tumor therapy in clinic. Tumor cells adapt to excessive oxidative stress by actuating reactive oxygen species (ROS)-defensing system, leading to a resistance to oxidation therapy. In this work, self-delivery photodynamic synergists (designated as PhotoSyn) are developed for oxidative damage amplified tumor therapy. Specifically, PhotoSyn are fabricated by the self-assembly of chlorine e6 (Ce6) and TH588 through π-π stacking and hydrophobic interactions. Without additional carriers, nanoscale PhotoSyn possess an extremely high drug loading rate (up to 100%) and they are found to be fairly stable in aqueous phase with a uniform size distribution. Intravenously injected PhotoSyn prefer to accumulate at tumor sites for effective cellular uptake. More importantly, TH588-mediated MTH1 inhibition could destroy the ROS-defensing system of tumor cells by preventing the elimination of 8-oxo-2'-deoxyguanosine triphosphate (8-oxo-dG), thereby exacerbating the oxidative DNA damage induced by the photodynamic therapy (PDT) of Ce6 under light irradiation. As a consequence, PhotoSyn exhibit enhanced photo toxicity and a significant antitumor effect. This amplified oxidative damage strategy improves the PDT efficiency with a reduced side effect by increasing the lethality of ROS without generating superabundant ROS, which would provide a new insight for developing self-delivery nanoplatforms in photodynamic tumor therapy in clinic.Tumor cells adapt to excessive oxidative stress by actuating reactive oxygen species (ROS)-defensing system, leading to a resistance to oxidation therapy. In this work, self-delivery photodynamic synergists (designated as PhotoSyn) are developed for oxidative damage amplified tumor therapy. Specifically, PhotoSyn are fabricated by the self-assembly of chlorine e6 (Ce6) and TH588 through π-π stacking and hydrophobic interactions. Without additional carriers, nanoscale PhotoSyn possess an extremely high drug loading rate (up to 100%) and they are found to be fairly stable in aqueous phase with a uniform size distribution. Intravenously injected PhotoSyn prefer to accumulate at tumor sites for effective cellular uptake. More importantly, TH588-mediated MTH1 inhibition could destroy the ROS-defensing system of tumor cells by preventing the elimination of 8-oxo-2'-deoxyguanosine triphosphate (8-oxo-dG), thereby exacerbating the oxidative DNA damage induced by the photodynamic therapy (PDT) of Ce6 under light irradiation. As a consequence, PhotoSyn exhibit enhanced photo toxicity and a significant antitumor effect. This amplified oxidative damage strategy improves the PDT efficiency with a reduced side effect by increasing the lethality of ROS without generating superabundant ROS, which would provide a new insight for developing self-delivery nanoplatforms in photodynamic tumor therapy in clinic. Tumor cells adapt to excessive oxidative stress by actuating reactive oxygen species (ROS)‐defensing system, leading to a resistance to oxidation therapy. In this work, self‐delivery photodynamic synergists (designated as PhotoSyn) are developed for oxidative damage amplified tumor therapy. Specifically, PhotoSyn are fabricated by the self‐assembly of chlorine e6 (Ce6) and TH588 through π–π stacking and hydrophobic interactions. Without additional carriers, nanoscale PhotoSyn possess an extremely high drug loading rate (up to 100%) and they are found to be fairly stable in aqueous phase with a uniform size distribution. Intravenously injected PhotoSyn prefer to accumulate at tumor sites for effective cellular uptake. More importantly, TH588‐mediated MTH1 inhibition could destroy the ROS‐defensing system of tumor cells by preventing the elimination of 8‐oxo‐2′‐deoxyguanosine triphosphate (8‐oxo‐dG), thereby exacerbating the oxidative DNA damage induced by the photodynamic therapy (PDT) of Ce6 under light irradiation. As a consequence, PhotoSyn exhibit enhanced photo toxicity and a significant antitumor effect. This amplified oxidative damage strategy improves the PDT efficiency with a reduced side effect by increasing the lethality of ROS without generating superabundant ROS, which would provide a new insight for developing self‐delivery nanoplatforms in photodynamic tumor therapy in clinic. Carrier free photodynamic synergists are developed for oxidative damage amplified tumor therapy by destroying the reactive oxygen species (ROS)‐defensing system without generating excessive ROS, which shed light on the development of self‐delivery nanoplatforms for efficient photodynamic therapy by utilizing the limited oxygen in hypoxic tumors. |
| Author | Liu, Yi‐Bin Cheng, Hong Li, Xin‐Yu Yu, Xi‐Yong Liu, Ling‐Shan Chen, A‐Li Zheng, Rong‐Rong Deng, Fu‐An Kong, Ren‐Jiang Li, Shi‐Ying |
| Author_xml | – sequence: 1 givenname: Xin‐Yu surname: Li fullname: Li, Xin‐Yu organization: Southern Medical University – sequence: 2 givenname: Fu‐An surname: Deng fullname: Deng, Fu‐An organization: Guangzhou Medical University – sequence: 3 givenname: Rong‐Rong surname: Zheng fullname: Zheng, Rong‐Rong organization: Guangzhou Medical University – sequence: 4 givenname: Ling‐Shan surname: Liu fullname: Liu, Ling‐Shan organization: Southern Medical University – sequence: 5 givenname: Yi‐Bin surname: Liu fullname: Liu, Yi‐Bin organization: Guangzhou Medical University – sequence: 6 givenname: Ren‐Jiang surname: Kong fullname: Kong, Ren‐Jiang organization: Southern Medical University – sequence: 7 givenname: A‐Li surname: Chen fullname: Chen, A‐Li organization: Guangzhou Medical University – sequence: 8 givenname: Xi‐Yong surname: Yu fullname: Yu, Xi‐Yong organization: Guangzhou Medical University – sequence: 9 givenname: Shi‐Ying surname: Li fullname: Li, Shi‐Ying email: lisy-sci@gzhmu.edu.cn organization: Guangzhou Medical University – sequence: 10 givenname: Hong orcidid: 0000-0002-3560-4432 surname: Cheng fullname: Cheng, Hong email: chengh@smu.edu.cn organization: Southern Medical University |
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| Snippet | Tumor cells adapt to excessive oxidative stress by actuating reactive oxygen species (ROS)‐defensing system, leading to a resistance to oxidation therapy. In... Tumor cells adapt to excessive oxidative stress by actuating reactive oxygen species (ROS)-defensing system, leading to a resistance to oxidation therapy. In... |
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| StartPage | e2102470 |
| SubjectTerms | Anticancer properties Chlorine Hydrophobicity Lethality Light irradiation Loading rate MTH1 inhibition nanoplatform Nanotechnology Oxidation resistance oxidative damage Photodynamic therapy Radiation damage self‐delivery Size distribution Toxicity |
| Title | Carrier Free Photodynamic Synergists for Oxidative Damage Amplified Tumor Therapy |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fsmll.202102470 https://www.proquest.com/docview/2579307914 https://www.proquest.com/docview/2569374190 |
| Volume | 17 |
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