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. 2022 Jul 16;20:329. doi: 10.1186/s12951-022-01531-5

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Scheme 1 — Schematic illustration of the triple action NP@Pt-1 for chemotherapy, PDT and cancer immunotherapy. A Chemical structures of Pt-1 and the ROS sensitive polymer carrier (P1) and their assembly into NP@Pt-1. B Illustration of the triple action of NP@Pt-1. NP@Pt-1 were injected to CT-26 tumor bearing mice and were then accumulated to the tumor site. Under light irradiation (420 nm), numerous ROS was generated to break down the polymer chain (thioketal bonds), resulting in the release of Pt-1. Pt-1 then chelated with intracellular DNA to induce apoptosis for chemotherapy. Moreover, the ROS can on the one hand damage the cell membranes, proteins and DNAs in cancer cells for PDT. On the other hand, it can induce ICD effect by sending out “eat me” signal for cancer immunotherapy