Loading…

Cascade Bioreactors Based on Host–Guest Molecular Inclusion Complexes for Triple‐Negative Breast Cancer Therapy via Inducing Ferroptosis

Triple‐negative breast cancer (TNBC) poses significant challenges in tumor treatment. Ferroptosis, as a novel cell death mechanism, holds promise as a potential therapeutic strategy for TNBC. In this study, cascade bioreactors based on host–guest molecular inclusion complexes (PCFP@PL/p53) are const...

Full description

Saved in:
Bibliographic Details
Published in:Advanced functional materials 2024-03, Vol.34 (12), p.n/a
Main Authors: Jia, Zengguang, Zhang, Jun, Wei, Yawen, Pan, Xiuhua, Hu, Zongwei, Kang, Ruixin, Zhou, Xiawei, Shen, Qi
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites cdi_FETCH-LOGICAL-c2727-dba3ed97bd55c12a613aa736ca2e851d49a484c7c15d530946a5577b200e55d53
container_end_page n/a
container_issue 12
container_start_page
container_title Advanced functional materials
container_volume 34
creator Jia, Zengguang
Zhang, Jun
Wei, Yawen
Pan, Xiuhua
Hu, Zongwei
Kang, Ruixin
Zhou, Xiawei
Shen, Qi
description Triple‐negative breast cancer (TNBC) poses significant challenges in tumor treatment. Ferroptosis, as a novel cell death mechanism, holds promise as a potential therapeutic strategy for TNBC. In this study, cascade bioreactors based on host–guest molecular inclusion complexes (PCFP@PL/p53) are constructed for TNBC therapy via inducing ferroptosis. The bioreactors are composed of hydrophobic hemirotaxane (mPEG‐β‐CD/α‐CD) and hydrophilic multi‐branched polyethyleneimine‐ferrocene (PEI‐Fc). They are linked by the reactive oxygen species (ROS)‐responsive molecular switch β‐CD@Fc, which can be activated by high levels of ROS. This activation leads to the rapid disassembly of PCFP@PL/p53 and the subsequent release of the loaded piperlongumine (PL) and p53 plasmids. In addition to acting as a “switch,” Fc can react with hydrogen peroxide (H2O2) in a Fenton reaction to produce hydroxyl radicals. PL decreases intracellular reduced glutathione and induces H2O2 accumulation, which corporates with Fc to launch ferroptosis and activated p53. The activated p53 disrupts the SLC7A11‐GSH‐GPX4 pathway, further increasing the intracellular ROS levels, resulting in a cascade amplification of ROS that ultimately induces massive ferroptosis. Meanwhile, the PCFP@PL/p53‐induced ferroptosis also activates the immune system in vivo, restricting the growth and metastasis of TNBC, thus providing a novel approach for TNBC therapy based on ferroptosis. PCFP@PL/p53 not only responds to reactive oxygen species (ROS) and releases piperlongumine (PL) and ferrocene for Fenton reaction acceleration and ROS enhancement but also induces ferroptosis through a cascade amplifying effect of ROS integrating with p53. The ferroptosis caused by PCFP@PL/p53 activates the anti‐tumor immune response, which further strengthens the therapeutic effect based on ferroptosis in triple‐negative breast cancer.
doi_str_mv 10.1002/adfm.202309727
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2968690231</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2968690231</sourcerecordid><originalsourceid>FETCH-LOGICAL-c2727-dba3ed97bd55c12a613aa736ca2e851d49a484c7c15d530946a5577b200e55d53</originalsourceid><addsrcrecordid>eNqFkDtPwzAUhSMEEuWxMltibrGdh5OxDbRF4rGAxBbd2jdglMbBTgrd-AEMSPxDfgmOisrIZPv6nHN1viA4YXTEKOVnoMrliFMe0kxwsRMMWMKSYUh5uru9s4f94MC5Z0qZEGE0CD5ycBIUkok2FkG2xjoyAYeKmJrMjWu_379mHbqWXJsKZVeBJZe1rDqnvSA3y6bCN3SkNJbcWe1f3--fN_gIrV75VJ_prTnUEv3_E1po1mSlwWeoTur6kUzRWtO0xml3FOyVUDk8_j0Pg_vpxV0-H17dzi7z8dVQct9sqBYQosrEQsWxZBwSFgKIMJHAMY2ZijKI0kgKyWIVexpRAnEsxIJTinE_OgxON7mNNS99t-LZdLb2KwueJWmSeYjMq0YblbTGOYtl0Vi9BLsuGC164kVPvNgS94ZsY3jVFa7_URfj8-n1n_cHKd6I0g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2968690231</pqid></control><display><type>article</type><title>Cascade Bioreactors Based on Host–Guest Molecular Inclusion Complexes for Triple‐Negative Breast Cancer Therapy via Inducing Ferroptosis</title><source>Wiley-Blackwell Read &amp; Publish Collection</source><creator>Jia, Zengguang ; Zhang, Jun ; Wei, Yawen ; Pan, Xiuhua ; Hu, Zongwei ; Kang, Ruixin ; Zhou, Xiawei ; Shen, Qi</creator><creatorcontrib>Jia, Zengguang ; Zhang, Jun ; Wei, Yawen ; Pan, Xiuhua ; Hu, Zongwei ; Kang, Ruixin ; Zhou, Xiawei ; Shen, Qi</creatorcontrib><description>Triple‐negative breast cancer (TNBC) poses significant challenges in tumor treatment. Ferroptosis, as a novel cell death mechanism, holds promise as a potential therapeutic strategy for TNBC. In this study, cascade bioreactors based on host–guest molecular inclusion complexes (PCFP@PL/p53) are constructed for TNBC therapy via inducing ferroptosis. The bioreactors are composed of hydrophobic hemirotaxane (mPEG‐β‐CD/α‐CD) and hydrophilic multi‐branched polyethyleneimine‐ferrocene (PEI‐Fc). They are linked by the reactive oxygen species (ROS)‐responsive molecular switch β‐CD@Fc, which can be activated by high levels of ROS. This activation leads to the rapid disassembly of PCFP@PL/p53 and the subsequent release of the loaded piperlongumine (PL) and p53 plasmids. In addition to acting as a “switch,” Fc can react with hydrogen peroxide (H2O2) in a Fenton reaction to produce hydroxyl radicals. PL decreases intracellular reduced glutathione and induces H2O2 accumulation, which corporates with Fc to launch ferroptosis and activated p53. The activated p53 disrupts the SLC7A11‐GSH‐GPX4 pathway, further increasing the intracellular ROS levels, resulting in a cascade amplification of ROS that ultimately induces massive ferroptosis. Meanwhile, the PCFP@PL/p53‐induced ferroptosis also activates the immune system in vivo, restricting the growth and metastasis of TNBC, thus providing a novel approach for TNBC therapy based on ferroptosis. PCFP@PL/p53 not only responds to reactive oxygen species (ROS) and releases piperlongumine (PL) and ferrocene for Fenton reaction acceleration and ROS enhancement but also induces ferroptosis through a cascade amplifying effect of ROS integrating with p53. The ferroptosis caused by PCFP@PL/p53 activates the anti‐tumor immune response, which further strengthens the therapeutic effect based on ferroptosis in triple‐negative breast cancer.</description><identifier>ISSN: 1616-301X</identifier><identifier>EISSN: 1616-3028</identifier><identifier>DOI: 10.1002/adfm.202309727</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc</publisher><subject>Bioreactors ; Breast cancer ; cascade bioreactors ; Cell death ; Ferroptosis ; Glutathione ; host–guest molecular inclusion complexes ; Hydrogen peroxide ; Hydroxyl radicals ; Immune system ; Inclusion complexes ; Molecular machines ; p53 ; piperlongumine ; Polyethyleneimine ; Supramolecular compounds ; Therapy</subject><ispartof>Advanced functional materials, 2024-03, Vol.34 (12), p.n/a</ispartof><rights>2023 Wiley‐VCH GmbH</rights><rights>2024 Wiley‐VCH GmbH</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c2727-dba3ed97bd55c12a613aa736ca2e851d49a484c7c15d530946a5577b200e55d53</cites><orcidid>0000-0003-1509-5391</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Jia, Zengguang</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><creatorcontrib>Wei, Yawen</creatorcontrib><creatorcontrib>Pan, Xiuhua</creatorcontrib><creatorcontrib>Hu, Zongwei</creatorcontrib><creatorcontrib>Kang, Ruixin</creatorcontrib><creatorcontrib>Zhou, Xiawei</creatorcontrib><creatorcontrib>Shen, Qi</creatorcontrib><title>Cascade Bioreactors Based on Host–Guest Molecular Inclusion Complexes for Triple‐Negative Breast Cancer Therapy via Inducing Ferroptosis</title><title>Advanced functional materials</title><description>Triple‐negative breast cancer (TNBC) poses significant challenges in tumor treatment. Ferroptosis, as a novel cell death mechanism, holds promise as a potential therapeutic strategy for TNBC. In this study, cascade bioreactors based on host–guest molecular inclusion complexes (PCFP@PL/p53) are constructed for TNBC therapy via inducing ferroptosis. The bioreactors are composed of hydrophobic hemirotaxane (mPEG‐β‐CD/α‐CD) and hydrophilic multi‐branched polyethyleneimine‐ferrocene (PEI‐Fc). They are linked by the reactive oxygen species (ROS)‐responsive molecular switch β‐CD@Fc, which can be activated by high levels of ROS. This activation leads to the rapid disassembly of PCFP@PL/p53 and the subsequent release of the loaded piperlongumine (PL) and p53 plasmids. In addition to acting as a “switch,” Fc can react with hydrogen peroxide (H2O2) in a Fenton reaction to produce hydroxyl radicals. PL decreases intracellular reduced glutathione and induces H2O2 accumulation, which corporates with Fc to launch ferroptosis and activated p53. The activated p53 disrupts the SLC7A11‐GSH‐GPX4 pathway, further increasing the intracellular ROS levels, resulting in a cascade amplification of ROS that ultimately induces massive ferroptosis. Meanwhile, the PCFP@PL/p53‐induced ferroptosis also activates the immune system in vivo, restricting the growth and metastasis of TNBC, thus providing a novel approach for TNBC therapy based on ferroptosis. PCFP@PL/p53 not only responds to reactive oxygen species (ROS) and releases piperlongumine (PL) and ferrocene for Fenton reaction acceleration and ROS enhancement but also induces ferroptosis through a cascade amplifying effect of ROS integrating with p53. The ferroptosis caused by PCFP@PL/p53 activates the anti‐tumor immune response, which further strengthens the therapeutic effect based on ferroptosis in triple‐negative breast cancer.</description><subject>Bioreactors</subject><subject>Breast cancer</subject><subject>cascade bioreactors</subject><subject>Cell death</subject><subject>Ferroptosis</subject><subject>Glutathione</subject><subject>host–guest molecular inclusion complexes</subject><subject>Hydrogen peroxide</subject><subject>Hydroxyl radicals</subject><subject>Immune system</subject><subject>Inclusion complexes</subject><subject>Molecular machines</subject><subject>p53</subject><subject>piperlongumine</subject><subject>Polyethyleneimine</subject><subject>Supramolecular compounds</subject><subject>Therapy</subject><issn>1616-301X</issn><issn>1616-3028</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNqFkDtPwzAUhSMEEuWxMltibrGdh5OxDbRF4rGAxBbd2jdglMbBTgrd-AEMSPxDfgmOisrIZPv6nHN1viA4YXTEKOVnoMrliFMe0kxwsRMMWMKSYUh5uru9s4f94MC5Z0qZEGE0CD5ycBIUkok2FkG2xjoyAYeKmJrMjWu_379mHbqWXJsKZVeBJZe1rDqnvSA3y6bCN3SkNJbcWe1f3--fN_gIrV75VJ_prTnUEv3_E1po1mSlwWeoTur6kUzRWtO0xml3FOyVUDk8_j0Pg_vpxV0-H17dzi7z8dVQct9sqBYQosrEQsWxZBwSFgKIMJHAMY2ZijKI0kgKyWIVexpRAnEsxIJTinE_OgxON7mNNS99t-LZdLb2KwueJWmSeYjMq0YblbTGOYtl0Vi9BLsuGC164kVPvNgS94ZsY3jVFa7_URfj8-n1n_cHKd6I0g</recordid><startdate>20240301</startdate><enddate>20240301</enddate><creator>Jia, Zengguang</creator><creator>Zhang, Jun</creator><creator>Wei, Yawen</creator><creator>Pan, Xiuhua</creator><creator>Hu, Zongwei</creator><creator>Kang, Ruixin</creator><creator>Zhou, Xiawei</creator><creator>Shen, Qi</creator><general>Wiley Subscription Services, Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7SP</scope><scope>7SR</scope><scope>7U5</scope><scope>8BQ</scope><scope>8FD</scope><scope>JG9</scope><scope>L7M</scope><orcidid>https://orcid.org/0000-0003-1509-5391</orcidid></search><sort><creationdate>20240301</creationdate><title>Cascade Bioreactors Based on Host–Guest Molecular Inclusion Complexes for Triple‐Negative Breast Cancer Therapy via Inducing Ferroptosis</title><author>Jia, Zengguang ; Zhang, Jun ; Wei, Yawen ; Pan, Xiuhua ; Hu, Zongwei ; Kang, Ruixin ; Zhou, Xiawei ; Shen, Qi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2727-dba3ed97bd55c12a613aa736ca2e851d49a484c7c15d530946a5577b200e55d53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Bioreactors</topic><topic>Breast cancer</topic><topic>cascade bioreactors</topic><topic>Cell death</topic><topic>Ferroptosis</topic><topic>Glutathione</topic><topic>host–guest molecular inclusion complexes</topic><topic>Hydrogen peroxide</topic><topic>Hydroxyl radicals</topic><topic>Immune system</topic><topic>Inclusion complexes</topic><topic>Molecular machines</topic><topic>p53</topic><topic>piperlongumine</topic><topic>Polyethyleneimine</topic><topic>Supramolecular compounds</topic><topic>Therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jia, Zengguang</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><creatorcontrib>Wei, Yawen</creatorcontrib><creatorcontrib>Pan, Xiuhua</creatorcontrib><creatorcontrib>Hu, Zongwei</creatorcontrib><creatorcontrib>Kang, Ruixin</creatorcontrib><creatorcontrib>Zhou, Xiawei</creatorcontrib><creatorcontrib>Shen, Qi</creatorcontrib><collection>CrossRef</collection><collection>Electronics &amp; Communications Abstracts</collection><collection>Engineered Materials Abstracts</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>METADEX</collection><collection>Technology Research Database</collection><collection>Materials Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><jtitle>Advanced functional materials</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jia, Zengguang</au><au>Zhang, Jun</au><au>Wei, Yawen</au><au>Pan, Xiuhua</au><au>Hu, Zongwei</au><au>Kang, Ruixin</au><au>Zhou, Xiawei</au><au>Shen, Qi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cascade Bioreactors Based on Host–Guest Molecular Inclusion Complexes for Triple‐Negative Breast Cancer Therapy via Inducing Ferroptosis</atitle><jtitle>Advanced functional materials</jtitle><date>2024-03-01</date><risdate>2024</risdate><volume>34</volume><issue>12</issue><epage>n/a</epage><issn>1616-301X</issn><eissn>1616-3028</eissn><abstract>Triple‐negative breast cancer (TNBC) poses significant challenges in tumor treatment. Ferroptosis, as a novel cell death mechanism, holds promise as a potential therapeutic strategy for TNBC. In this study, cascade bioreactors based on host–guest molecular inclusion complexes (PCFP@PL/p53) are constructed for TNBC therapy via inducing ferroptosis. The bioreactors are composed of hydrophobic hemirotaxane (mPEG‐β‐CD/α‐CD) and hydrophilic multi‐branched polyethyleneimine‐ferrocene (PEI‐Fc). They are linked by the reactive oxygen species (ROS)‐responsive molecular switch β‐CD@Fc, which can be activated by high levels of ROS. This activation leads to the rapid disassembly of PCFP@PL/p53 and the subsequent release of the loaded piperlongumine (PL) and p53 plasmids. In addition to acting as a “switch,” Fc can react with hydrogen peroxide (H2O2) in a Fenton reaction to produce hydroxyl radicals. PL decreases intracellular reduced glutathione and induces H2O2 accumulation, which corporates with Fc to launch ferroptosis and activated p53. The activated p53 disrupts the SLC7A11‐GSH‐GPX4 pathway, further increasing the intracellular ROS levels, resulting in a cascade amplification of ROS that ultimately induces massive ferroptosis. Meanwhile, the PCFP@PL/p53‐induced ferroptosis also activates the immune system in vivo, restricting the growth and metastasis of TNBC, thus providing a novel approach for TNBC therapy based on ferroptosis. PCFP@PL/p53 not only responds to reactive oxygen species (ROS) and releases piperlongumine (PL) and ferrocene for Fenton reaction acceleration and ROS enhancement but also induces ferroptosis through a cascade amplifying effect of ROS integrating with p53. The ferroptosis caused by PCFP@PL/p53 activates the anti‐tumor immune response, which further strengthens the therapeutic effect based on ferroptosis in triple‐negative breast cancer.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc</pub><doi>10.1002/adfm.202309727</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0003-1509-5391</orcidid></addata></record>
fulltext fulltext
identifier ISSN: 1616-301X
ispartof Advanced functional materials, 2024-03, Vol.34 (12), p.n/a
issn 1616-301X
1616-3028
language eng
recordid cdi_proquest_journals_2968690231
source Wiley-Blackwell Read & Publish Collection
subjects Bioreactors
Breast cancer
cascade bioreactors
Cell death
Ferroptosis
Glutathione
host–guest molecular inclusion complexes
Hydrogen peroxide
Hydroxyl radicals
Immune system
Inclusion complexes
Molecular machines
p53
piperlongumine
Polyethyleneimine
Supramolecular compounds
Therapy
title Cascade Bioreactors Based on Host–Guest Molecular Inclusion Complexes for Triple‐Negative Breast Cancer Therapy via Inducing Ferroptosis
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T06%3A49%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cascade%20Bioreactors%20Based%20on%20Host%E2%80%93Guest%20Molecular%20Inclusion%20Complexes%20for%20Triple%E2%80%90Negative%20Breast%20Cancer%20Therapy%20via%20Inducing%20Ferroptosis&rft.jtitle=Advanced%20functional%20materials&rft.au=Jia,%20Zengguang&rft.date=2024-03-01&rft.volume=34&rft.issue=12&rft.epage=n/a&rft.issn=1616-301X&rft.eissn=1616-3028&rft_id=info:doi/10.1002/adfm.202309727&rft_dat=%3Cproquest_cross%3E2968690231%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c2727-dba3ed97bd55c12a613aa736ca2e851d49a484c7c15d530946a5577b200e55d53%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2968690231&rft_id=info:pmid/&rfr_iscdi=true