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Ferroptosis Inducers in Thyroid Cancer
Purpose Papillary thyroid carcinoma (PTC) progression imparts reduced patient survival. Tumor resistance and progression can be influenced by Glutathione (GSH) metabolism. Glutathione peroxidase 4 (GPX4) regulates GSH oxidation to prevent lipid peroxidation of cell membranes during increased oxidati...
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| Published in: | World journal of surgery 2023-02, Vol.47 (2), p.371-381 |
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| Language: | English |
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| cites | cdi_FETCH-LOGICAL-c4266-8a08cb611c088b9747564244f3af0d065dae4afdc21b3228cb57f281ea0124673 |
| container_end_page | 381 |
| container_issue | 2 |
| container_start_page | 371 |
| container_title | World journal of surgery |
| container_volume | 47 |
| creator | Sekhar, Konjeti R. Cyr, Sriram Baregamian, Naira |
| description | Purpose
Papillary thyroid carcinoma (PTC) progression imparts reduced patient survival. Tumor resistance and progression can be influenced by Glutathione (GSH) metabolism. Glutathione peroxidase 4 (GPX4) regulates GSH oxidation to prevent lipid peroxidation of cell membranes during increased oxidative stress and regulates ferroptosis cell death pathway in tumor cells. This study examines the differential ferroptosis effects by GPX4 inhibitors in thyroid cancer cell and 3-D spheroid in vitro models.
Materials and methods
We examined differential effects of GPX4 inhibitors on PTC cells (K1, MDA-T32, MDA-T68) with BRAF and RAS mutations, and TERT promoter and PIK3CA co-mutations. The effects of GPX4 inhibitors on ferroptosis activation, proliferation, oxidative stress, and activation of signaling pathways were assessed by Western blot, total (GSH) and oxidized glutathione (GSSG) levels, ROS induction, RT-qPCR, migration, and proliferation assays.
Results
GPX4 inhibitors induced ferroptosis, rising ROS, GSH depletion, arrested tumor cell migration, increased DNA damage, suppressed mTOR pathway and DNA repair response in PTC cells in vitro. Differential responses to DNA damage and GPX4 levels were observed between 3-D PTC spheroids and thyroid cancer cells in a monolayer model.
Conclusion
Effective GPX4 inhibition with various inhibitors induced a robust but differential activation of ferroptosis in monolayer thyroid tumor cell and 3-D PTC spheroid models. Our study is the first of its kind to determine the differential effects of GPX4 inhibitors on thyroid cancer cells with diverse mutational signatures. We have identified a novel mechanism of action of GPX4 inhibition in preclinical in vitro models of thyroid cancer that can be further exploited for therapeutic benefit in advanced therapy-resistant thyroid cancers. |
| doi_str_mv | 10.1007/s00268-022-06738-z |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2721636363</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2721636363</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4266-8a08cb611c088b9747564244f3af0d065dae4afdc21b3228cb57f281ea0124673</originalsourceid><addsrcrecordid>eNqNkF1LwzAUhoMobn78AS9kIIg31ZOTNEm90-F0MvDCiZcha1Pt6NqZrMj2683sVPBCJBcJ4XkP73kIOaJwTgHkhQdAoSJAjEBIpqLVFulSzjBChmybdIEJHt6Udcie91MAKgWIXdJhgiaxkKpLTgfWuXq-qH3he8Mqa1LrfK-oeuPXpauLrNc3Vfg6IDu5Kb093Nz75GlwM-7fRaOH22H_ahSlHIWIlAGVTgSlKSg1SSSXseDIec5MDhmIODOWmzxLkU4YYmBjmaOi1gBFHnbYJ2ft3Lmr3xrrF3pW-NSWpals3XiNEqlg6xPQk1_otG5cFdoFKk44RymTQGFLpa723tlcz10xM26pKei1Rd1a1MGi_rSoVyF0vBndTGY2-458aQvAZQu8F6Vd_mOkfr5_vB4E_0qEMGvDPuSqF-t-iv_R6QMcbYwI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2759442779</pqid></control><display><type>article</type><title>Ferroptosis Inducers in Thyroid Cancer</title><source>Springer Link</source><creator>Sekhar, Konjeti R. ; Cyr, Sriram ; Baregamian, Naira</creator><creatorcontrib>Sekhar, Konjeti R. ; Cyr, Sriram ; Baregamian, Naira</creatorcontrib><description>Purpose
Papillary thyroid carcinoma (PTC) progression imparts reduced patient survival. Tumor resistance and progression can be influenced by Glutathione (GSH) metabolism. Glutathione peroxidase 4 (GPX4) regulates GSH oxidation to prevent lipid peroxidation of cell membranes during increased oxidative stress and regulates ferroptosis cell death pathway in tumor cells. This study examines the differential ferroptosis effects by GPX4 inhibitors in thyroid cancer cell and 3-D spheroid in vitro models.
Materials and methods
We examined differential effects of GPX4 inhibitors on PTC cells (K1, MDA-T32, MDA-T68) with BRAF and RAS mutations, and TERT promoter and PIK3CA co-mutations. The effects of GPX4 inhibitors on ferroptosis activation, proliferation, oxidative stress, and activation of signaling pathways were assessed by Western blot, total (GSH) and oxidized glutathione (GSSG) levels, ROS induction, RT-qPCR, migration, and proliferation assays.
Results
GPX4 inhibitors induced ferroptosis, rising ROS, GSH depletion, arrested tumor cell migration, increased DNA damage, suppressed mTOR pathway and DNA repair response in PTC cells in vitro. Differential responses to DNA damage and GPX4 levels were observed between 3-D PTC spheroids and thyroid cancer cells in a monolayer model.
Conclusion
Effective GPX4 inhibition with various inhibitors induced a robust but differential activation of ferroptosis in monolayer thyroid tumor cell and 3-D PTC spheroid models. Our study is the first of its kind to determine the differential effects of GPX4 inhibitors on thyroid cancer cells with diverse mutational signatures. We have identified a novel mechanism of action of GPX4 inhibition in preclinical in vitro models of thyroid cancer that can be further exploited for therapeutic benefit in advanced therapy-resistant thyroid cancers.</description><identifier>ISSN: 0364-2313</identifier><identifier>EISSN: 1432-2323</identifier><identifier>DOI: 10.1007/s00268-022-06738-z</identifier><identifier>PMID: 36195678</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Abdominal Surgery ; Cancer ; Cardiac Surgery ; Cell death ; Cell membranes ; Cell migration ; Damage ; Deoxyribonucleic acid ; Depletion ; DNA ; DNA damage ; DNA repair ; Ferroptosis ; General Surgery ; Glutathione ; Glutathione peroxidase ; Glutathione Peroxidase - genetics ; Glutathione Peroxidase - metabolism ; Humans ; In vitro methods and tests ; Inhibitors ; Lipid peroxidation ; Lipids ; Medicine ; Medicine & Public Health ; Metabolism ; Monolayers ; Mutation ; Original Scientific Report ; Oxidation ; Oxidative stress ; Papillary thyroid carcinoma ; Peroxidase ; Peroxidation ; Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism ; Reactive Oxygen Species - metabolism ; Spheroids ; Surgery ; Thoracic Surgery ; Three dimensional models ; Thyroid ; Thyroid cancer ; Thyroid Neoplasms - drug therapy ; Thyroid Neoplasms - genetics ; TOR protein ; Tumor cells ; Tumors ; Vascular Surgery</subject><ispartof>World journal of surgery, 2023-02, Vol.47 (2), p.371-381</ispartof><rights>The Author(s) under exclusive licence to Société Internationale de Chirurgie 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023 The Author(s) under exclusive licence to Société Internationale de Chirurgie</rights><rights>2022. The Author(s) under exclusive licence to Société Internationale de Chirurgie.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4266-8a08cb611c088b9747564244f3af0d065dae4afdc21b3228cb57f281ea0124673</citedby><cites>FETCH-LOGICAL-c4266-8a08cb611c088b9747564244f3af0d065dae4afdc21b3228cb57f281ea0124673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36195678$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sekhar, Konjeti R.</creatorcontrib><creatorcontrib>Cyr, Sriram</creatorcontrib><creatorcontrib>Baregamian, Naira</creatorcontrib><title>Ferroptosis Inducers in Thyroid Cancer</title><title>World journal of surgery</title><addtitle>World J Surg</addtitle><addtitle>World J Surg</addtitle><description>Purpose
Papillary thyroid carcinoma (PTC) progression imparts reduced patient survival. Tumor resistance and progression can be influenced by Glutathione (GSH) metabolism. Glutathione peroxidase 4 (GPX4) regulates GSH oxidation to prevent lipid peroxidation of cell membranes during increased oxidative stress and regulates ferroptosis cell death pathway in tumor cells. This study examines the differential ferroptosis effects by GPX4 inhibitors in thyroid cancer cell and 3-D spheroid in vitro models.
Materials and methods
We examined differential effects of GPX4 inhibitors on PTC cells (K1, MDA-T32, MDA-T68) with BRAF and RAS mutations, and TERT promoter and PIK3CA co-mutations. The effects of GPX4 inhibitors on ferroptosis activation, proliferation, oxidative stress, and activation of signaling pathways were assessed by Western blot, total (GSH) and oxidized glutathione (GSSG) levels, ROS induction, RT-qPCR, migration, and proliferation assays.
Results
GPX4 inhibitors induced ferroptosis, rising ROS, GSH depletion, arrested tumor cell migration, increased DNA damage, suppressed mTOR pathway and DNA repair response in PTC cells in vitro. Differential responses to DNA damage and GPX4 levels were observed between 3-D PTC spheroids and thyroid cancer cells in a monolayer model.
Conclusion
Effective GPX4 inhibition with various inhibitors induced a robust but differential activation of ferroptosis in monolayer thyroid tumor cell and 3-D PTC spheroid models. Our study is the first of its kind to determine the differential effects of GPX4 inhibitors on thyroid cancer cells with diverse mutational signatures. We have identified a novel mechanism of action of GPX4 inhibition in preclinical in vitro models of thyroid cancer that can be further exploited for therapeutic benefit in advanced therapy-resistant thyroid cancers.</description><subject>Abdominal Surgery</subject><subject>Cancer</subject><subject>Cardiac Surgery</subject><subject>Cell death</subject><subject>Cell membranes</subject><subject>Cell migration</subject><subject>Damage</subject><subject>Deoxyribonucleic acid</subject><subject>Depletion</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA repair</subject><subject>Ferroptosis</subject><subject>General Surgery</subject><subject>Glutathione</subject><subject>Glutathione peroxidase</subject><subject>Glutathione Peroxidase - genetics</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>Humans</subject><subject>In vitro methods and tests</subject><subject>Inhibitors</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolism</subject><subject>Monolayers</subject><subject>Mutation</subject><subject>Original Scientific Report</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>Papillary thyroid carcinoma</subject><subject>Peroxidase</subject><subject>Peroxidation</subject><subject>Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Spheroids</subject><subject>Surgery</subject><subject>Thoracic Surgery</subject><subject>Three dimensional models</subject><subject>Thyroid</subject><subject>Thyroid cancer</subject><subject>Thyroid Neoplasms - drug therapy</subject><subject>Thyroid Neoplasms - genetics</subject><subject>TOR protein</subject><subject>Tumor cells</subject><subject>Tumors</subject><subject>Vascular Surgery</subject><issn>0364-2313</issn><issn>1432-2323</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNqNkF1LwzAUhoMobn78AS9kIIg31ZOTNEm90-F0MvDCiZcha1Pt6NqZrMj2683sVPBCJBcJ4XkP73kIOaJwTgHkhQdAoSJAjEBIpqLVFulSzjBChmybdIEJHt6Udcie91MAKgWIXdJhgiaxkKpLTgfWuXq-qH3he8Mqa1LrfK-oeuPXpauLrNc3Vfg6IDu5Kb093Nz75GlwM-7fRaOH22H_ahSlHIWIlAGVTgSlKSg1SSSXseDIec5MDhmIODOWmzxLkU4YYmBjmaOi1gBFHnbYJ2ft3Lmr3xrrF3pW-NSWpals3XiNEqlg6xPQk1_otG5cFdoFKk44RymTQGFLpa723tlcz10xM26pKei1Rd1a1MGi_rSoVyF0vBndTGY2-458aQvAZQu8F6Vd_mOkfr5_vB4E_0qEMGvDPuSqF-t-iv_R6QMcbYwI</recordid><startdate>202302</startdate><enddate>202302</enddate><creator>Sekhar, Konjeti R.</creator><creator>Cyr, Sriram</creator><creator>Baregamian, Naira</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QO</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>202302</creationdate><title>Ferroptosis Inducers in Thyroid Cancer</title><author>Sekhar, Konjeti R. ; Cyr, Sriram ; Baregamian, Naira</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4266-8a08cb611c088b9747564244f3af0d065dae4afdc21b3228cb57f281ea0124673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Abdominal Surgery</topic><topic>Cancer</topic><topic>Cardiac Surgery</topic><topic>Cell death</topic><topic>Cell membranes</topic><topic>Cell migration</topic><topic>Damage</topic><topic>Deoxyribonucleic acid</topic><topic>Depletion</topic><topic>DNA</topic><topic>DNA damage</topic><topic>DNA repair</topic><topic>Ferroptosis</topic><topic>General Surgery</topic><topic>Glutathione</topic><topic>Glutathione peroxidase</topic><topic>Glutathione Peroxidase - genetics</topic><topic>Glutathione Peroxidase - metabolism</topic><topic>Humans</topic><topic>In vitro methods and tests</topic><topic>Inhibitors</topic><topic>Lipid peroxidation</topic><topic>Lipids</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolism</topic><topic>Monolayers</topic><topic>Mutation</topic><topic>Original Scientific Report</topic><topic>Oxidation</topic><topic>Oxidative stress</topic><topic>Papillary thyroid carcinoma</topic><topic>Peroxidase</topic><topic>Peroxidation</topic><topic>Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Spheroids</topic><topic>Surgery</topic><topic>Thoracic Surgery</topic><topic>Three dimensional models</topic><topic>Thyroid</topic><topic>Thyroid cancer</topic><topic>Thyroid Neoplasms - drug therapy</topic><topic>Thyroid Neoplasms - genetics</topic><topic>TOR protein</topic><topic>Tumor cells</topic><topic>Tumors</topic><topic>Vascular Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sekhar, Konjeti R.</creatorcontrib><creatorcontrib>Cyr, Sriram</creatorcontrib><creatorcontrib>Baregamian, Naira</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Health Medical collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>World journal of surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sekhar, Konjeti R.</au><au>Cyr, Sriram</au><au>Baregamian, Naira</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ferroptosis Inducers in Thyroid Cancer</atitle><jtitle>World journal of surgery</jtitle><stitle>World J Surg</stitle><addtitle>World J Surg</addtitle><date>2023-02</date><risdate>2023</risdate><volume>47</volume><issue>2</issue><spage>371</spage><epage>381</epage><pages>371-381</pages><issn>0364-2313</issn><eissn>1432-2323</eissn><abstract>Purpose
Papillary thyroid carcinoma (PTC) progression imparts reduced patient survival. Tumor resistance and progression can be influenced by Glutathione (GSH) metabolism. Glutathione peroxidase 4 (GPX4) regulates GSH oxidation to prevent lipid peroxidation of cell membranes during increased oxidative stress and regulates ferroptosis cell death pathway in tumor cells. This study examines the differential ferroptosis effects by GPX4 inhibitors in thyroid cancer cell and 3-D spheroid in vitro models.
Materials and methods
We examined differential effects of GPX4 inhibitors on PTC cells (K1, MDA-T32, MDA-T68) with BRAF and RAS mutations, and TERT promoter and PIK3CA co-mutations. The effects of GPX4 inhibitors on ferroptosis activation, proliferation, oxidative stress, and activation of signaling pathways were assessed by Western blot, total (GSH) and oxidized glutathione (GSSG) levels, ROS induction, RT-qPCR, migration, and proliferation assays.
Results
GPX4 inhibitors induced ferroptosis, rising ROS, GSH depletion, arrested tumor cell migration, increased DNA damage, suppressed mTOR pathway and DNA repair response in PTC cells in vitro. Differential responses to DNA damage and GPX4 levels were observed between 3-D PTC spheroids and thyroid cancer cells in a monolayer model.
Conclusion
Effective GPX4 inhibition with various inhibitors induced a robust but differential activation of ferroptosis in monolayer thyroid tumor cell and 3-D PTC spheroid models. Our study is the first of its kind to determine the differential effects of GPX4 inhibitors on thyroid cancer cells with diverse mutational signatures. We have identified a novel mechanism of action of GPX4 inhibition in preclinical in vitro models of thyroid cancer that can be further exploited for therapeutic benefit in advanced therapy-resistant thyroid cancers.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>36195678</pmid><doi>10.1007/s00268-022-06738-z</doi><tpages>11</tpages></addata></record> |
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| subjects | Abdominal Surgery Cancer Cardiac Surgery Cell death Cell membranes Cell migration Damage Deoxyribonucleic acid Depletion DNA DNA damage DNA repair Ferroptosis General Surgery Glutathione Glutathione peroxidase Glutathione Peroxidase - genetics Glutathione Peroxidase - metabolism Humans In vitro methods and tests Inhibitors Lipid peroxidation Lipids Medicine Medicine & Public Health Metabolism Monolayers Mutation Original Scientific Report Oxidation Oxidative stress Papillary thyroid carcinoma Peroxidase Peroxidation Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism Reactive Oxygen Species - metabolism Spheroids Surgery Thoracic Surgery Three dimensional models Thyroid Thyroid cancer Thyroid Neoplasms - drug therapy Thyroid Neoplasms - genetics TOR protein Tumor cells Tumors Vascular Surgery |
| title | Ferroptosis Inducers in Thyroid Cancer |
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