Tumor-Associated Antigen xCT and Mutant-p53 as Molecular Targets for New Combinatorial Antitumor Strategies
The cystine/glutamate antiporter xCT is a tumor-associated antigen that has been newly identified in many cancer types. By participating in glutathione biosynthesis, xCT protects cancer cells from oxidative stress conditions and ferroptosis, and contributes to metabolic reprogramming, thus promoting...
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| Veröffentlicht in: | Cells (Basel, Switzerland) Switzerland), 2021-01, Vol.10 (1), p.108, Article 108 |
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| description | The cystine/glutamate antiporter xCT is a tumor-associated antigen that has been newly identified in many cancer types. By participating in glutathione biosynthesis, xCT protects cancer cells from oxidative stress conditions and ferroptosis, and contributes to metabolic reprogramming, thus promoting tumor progression and chemoresistance. Moreover, xCT is overexpressed in cancer stem cells. These features render xCT a promising target for cancer therapy, as has been widely reported in the literature and in our work on its immunotargeting. Interestingly, studies on the TP53 gene have revealed that both wild-type and mutant p53 induce the post-transcriptional down modulation of xCT, contributing to ferroptosis. Moreover, APR-246, a small molecule drug that can restore wild-type p53 function in cancer cells, has been described as an indirect modulator of xCT expression in tumors with mutant p53 accumulation, and is thus a promising drug to use in combination with xCT inhibition. This review summarizes the current knowledge of xCT and its regulation by p53, with a focus on the crosstalk of these two molecules in ferroptosis, and also considers some possible combinatorial strategies that can make use of APR-246 treatment in combination with anti-xCT immunotargeting. |
| doi_str_mv | 10.3390/cells10010108 |
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By participating in glutathione biosynthesis, xCT protects cancer cells from oxidative stress conditions and ferroptosis, and contributes to metabolic reprogramming, thus promoting tumor progression and chemoresistance. Moreover, xCT is overexpressed in cancer stem cells. These features render xCT a promising target for cancer therapy, as has been widely reported in the literature and in our work on its immunotargeting. Interestingly, studies on the TP53 gene have revealed that both wild-type and mutant p53 induce the post-transcriptional down modulation of xCT, contributing to ferroptosis. Moreover, APR-246, a small molecule drug that can restore wild-type p53 function in cancer cells, has been described as an indirect modulator of xCT expression in tumors with mutant p53 accumulation, and is thus a promising drug to use in combination with xCT inhibition. This review summarizes the current knowledge of xCT and its regulation by p53, with a focus on the crosstalk of these two molecules in ferroptosis, and also considers some possible combinatorial strategies that can make use of APR-246 treatment in combination with anti-xCT immunotargeting.</description><identifier>ISSN: 2073-4409</identifier><identifier>EISSN: 2073-4409</identifier><identifier>DOI: 10.3390/cells10010108</identifier><identifier>PMID: 33430127</identifier><language>eng</language><publisher>BASEL: Mdpi</publisher><subject>Amino Acid Transport System y+ - genetics ; Amino acids ; Animals ; Antigen (tumor-associated) ; Antineoplastic Agents - therapeutic use ; Antioxidants ; Antitumor agents ; Apoptosis ; APR-246 ; breast cancer ; Cancer ; Cancer therapies ; Cell adhesion & migration ; Cell Biology ; Chemoresistance ; Deoxyribonucleic acid ; DNA ; Ferroptosis ; Genes ; Glutathione ; Homeostasis ; Humans ; Life Sciences & Biomedicine ; Metabolism ; Metastasis ; Molecular Targeted Therapy ; Mutants ; Mutation - genetics ; Neoplasms - drug therapy ; Neoplasms - genetics ; Oxidative stress ; p53 ; p53 Protein ; Post-transcription ; PRIMA-1 ; Proteins ; Recovery of function ; Review ; Science & Technology ; Stem cells ; Transcription factors ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Tumors ; xCT</subject><ispartof>Cells (Basel, Switzerland), 2021-01, Vol.10 (1), p.108, Article 108</ispartof><rights>2021. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>16</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000609982600001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c481t-4afcee4cfff9459aee2709ee77401816f37d70f8cc9c9c29fa96a651450179693</citedby><cites>FETCH-LOGICAL-c481t-4afcee4cfff9459aee2709ee77401816f37d70f8cc9c9c29fa96a651450179693</cites><orcidid>0000-0003-1665-3594 ; 0000-0001-5698-0202 ; 0000-0003-1780-098X ; 0000-0003-4571-1060 ; 0000-0002-7224-347X ; 0000-0002-0431-2656</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7827209/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7827209/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2115,27929,27930,39263,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33430127$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Magri, Jolanda</creatorcontrib><creatorcontrib>Gasparetto, Alessandro</creatorcontrib><creatorcontrib>Conti, Laura</creatorcontrib><creatorcontrib>Calautti, Enzo</creatorcontrib><creatorcontrib>Cossu, Chiara</creatorcontrib><creatorcontrib>Ruiu, Roberto</creatorcontrib><creatorcontrib>Barutello, Giuseppina</creatorcontrib><creatorcontrib>Cavallo, Federica</creatorcontrib><title>Tumor-Associated Antigen xCT and Mutant-p53 as Molecular Targets for New Combinatorial Antitumor Strategies</title><title>Cells (Basel, Switzerland)</title><addtitle>CELLS-BASEL</addtitle><addtitle>Cells</addtitle><description>The cystine/glutamate antiporter xCT is a tumor-associated antigen that has been newly identified in many cancer types. 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This review summarizes the current knowledge of xCT and its regulation by p53, with a focus on the crosstalk of these two molecules in ferroptosis, and also considers some possible combinatorial strategies that can make use of APR-246 treatment in combination with anti-xCT immunotargeting.</description><subject>Amino Acid Transport System y+ - genetics</subject><subject>Amino acids</subject><subject>Animals</subject><subject>Antigen (tumor-associated)</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Antioxidants</subject><subject>Antitumor agents</subject><subject>Apoptosis</subject><subject>APR-246</subject><subject>breast cancer</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Chemoresistance</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Ferroptosis</subject><subject>Genes</subject><subject>Glutathione</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Life Sciences & Biomedicine</subject><subject>Metabolism</subject><subject>Metastasis</subject><subject>Molecular Targeted Therapy</subject><subject>Mutants</subject><subject>Mutation - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cells (Basel, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Magri, Jolanda</au><au>Gasparetto, Alessandro</au><au>Conti, Laura</au><au>Calautti, Enzo</au><au>Cossu, Chiara</au><au>Ruiu, Roberto</au><au>Barutello, Giuseppina</au><au>Cavallo, Federica</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor-Associated Antigen xCT and Mutant-p53 as Molecular Targets for New Combinatorial Antitumor Strategies</atitle><jtitle>Cells (Basel, Switzerland)</jtitle><stitle>CELLS-BASEL</stitle><addtitle>Cells</addtitle><date>2021-01-08</date><risdate>2021</risdate><volume>10</volume><issue>1</issue><spage>108</spage><pages>108-</pages><artnum>108</artnum><issn>2073-4409</issn><eissn>2073-4409</eissn><abstract>The cystine/glutamate antiporter xCT is a tumor-associated antigen that has been newly identified in many cancer types. 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This review summarizes the current knowledge of xCT and its regulation by p53, with a focus on the crosstalk of these two molecules in ferroptosis, and also considers some possible combinatorial strategies that can make use of APR-246 treatment in combination with anti-xCT immunotargeting.</abstract><cop>BASEL</cop><pub>Mdpi</pub><pmid>33430127</pmid><doi>10.3390/cells10010108</doi><tpages>21</tpages><orcidid>https://orcid.org/0000-0003-1665-3594</orcidid><orcidid>https://orcid.org/0000-0001-5698-0202</orcidid><orcidid>https://orcid.org/0000-0003-1780-098X</orcidid><orcidid>https://orcid.org/0000-0003-4571-1060</orcidid><orcidid>https://orcid.org/0000-0002-7224-347X</orcidid><orcidid>https://orcid.org/0000-0002-0431-2656</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; MDPI - Multidisciplinary Digital Publishing Institute; Web of Science - Science Citation Index Expanded - 2021<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" />; PubMed Central |
| subjects | Amino Acid Transport System y+ - genetics Amino acids Animals Antigen (tumor-associated) Antineoplastic Agents - therapeutic use Antioxidants Antitumor agents Apoptosis APR-246 breast cancer Cancer Cancer therapies Cell adhesion & migration Cell Biology Chemoresistance Deoxyribonucleic acid DNA Ferroptosis Genes Glutathione Homeostasis Humans Life Sciences & Biomedicine Metabolism Metastasis Molecular Targeted Therapy Mutants Mutation - genetics Neoplasms - drug therapy Neoplasms - genetics Oxidative stress p53 p53 Protein Post-transcription PRIMA-1 Proteins Recovery of function Review Science & Technology Stem cells Transcription factors Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumors xCT |
| title | Tumor-Associated Antigen xCT and Mutant-p53 as Molecular Targets for New Combinatorial Antitumor Strategies |
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