Jun Li, Pei-Ting Li, Wei Wu, Bo-Ni Ding, Yan-Guang Wen, Hai-Lin Cai, Shuang-Xi Liu, Tao Hong, Jian-Fei Zhang, Jian-Da Zhou, Li-Yuan Qian, Juan Du
{"title":"POU2F2介导的lncRNA PTPRG-AS1上调通过miR-376c-3p/SLC7A11轴抑制乳腺癌中的铁突变。","authors":"Jun Li, Pei-Ting Li, Wei Wu, Bo-Ni Ding, Yan-Guang Wen, Hai-Lin Cai, Shuang-Xi Liu, Tao Hong, Jian-Fei Zhang, Jian-Da Zhou, Li-Yuan Qian, Juan Du","doi":"10.2217/epi-2023-0100","DOIUrl":null,"url":null,"abstract":"<p><p><b>Background:</b> Triple-negative breast cancer (TNBC) is a subtype of BC with high rates of mortality. The mechanism of <i>PTPRG-AS1</i> in ferroptosis of TNBC was investigated. <b>Methods:</b> Chromatin immunoprecipitation and dual-luciferase reporter assays were used to measure intermolecular relationships. MTT and colony formation assays detected cell viability and proliferation. Kits detected Fe<sup>2+</sup> and reactive oxygen species levels. The role of PTPRG-AS1 in tumor growth was analyzed <i>in vivo</i>. <b>Results:</b> <i>PTPRG-AS1</i> was increased in TNBC tissues and cells. <i>PTPRG-AS1</i> silencing increased the reduction of glutathione and GPX4, increased Fe<sup>2+</sup> and reactive oxygen species in erastin-treated cells and inhibited proliferation. POU2F2 transcriptionally upregulated <i>PTPRG-AS1</i>. <i>PTPRG-AS1</i> targeted miR-376c-3p to upregulate <i>SLC7A11</i>. <i>PTPRG-AS1</i> knockdown suppressed tumor growth <i>in vivo</i>. <b>Conclusion:</b> POU2F2 transcriptionally activates <i>PTPRG-AS1</i> to modulate ferroptosis and proliferation by miR-376c-3p/SLC7A11, promoting TNBC.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"215-231"},"PeriodicalIF":2.6000,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"POU2F2-mediated upregulation of lncRNA <i>PTPRG-AS1</i> inhibits ferroptosis in breast cancer via miR-376c-3p/SLC7A11 axis.\",\"authors\":\"Jun Li, Pei-Ting Li, Wei Wu, Bo-Ni Ding, Yan-Guang Wen, Hai-Lin Cai, Shuang-Xi Liu, Tao Hong, Jian-Fei Zhang, Jian-Da Zhou, Li-Yuan Qian, Juan Du\",\"doi\":\"10.2217/epi-2023-0100\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p><b>Background:</b> Triple-negative breast cancer (TNBC) is a subtype of BC with high rates of mortality. The mechanism of <i>PTPRG-AS1</i> in ferroptosis of TNBC was investigated. <b>Methods:</b> Chromatin immunoprecipitation and dual-luciferase reporter assays were used to measure intermolecular relationships. MTT and colony formation assays detected cell viability and proliferation. Kits detected Fe<sup>2+</sup> and reactive oxygen species levels. The role of PTPRG-AS1 in tumor growth was analyzed <i>in vivo</i>. <b>Results:</b> <i>PTPRG-AS1</i> was increased in TNBC tissues and cells. <i>PTPRG-AS1</i> silencing increased the reduction of glutathione and GPX4, increased Fe<sup>2+</sup> and reactive oxygen species in erastin-treated cells and inhibited proliferation. POU2F2 transcriptionally upregulated <i>PTPRG-AS1</i>. <i>PTPRG-AS1</i> targeted miR-376c-3p to upregulate <i>SLC7A11</i>. <i>PTPRG-AS1</i> knockdown suppressed tumor growth <i>in vivo</i>. <b>Conclusion:</b> POU2F2 transcriptionally activates <i>PTPRG-AS1</i> to modulate ferroptosis and proliferation by miR-376c-3p/SLC7A11, promoting TNBC.</p>\",\"PeriodicalId\":11959,\"journal\":{\"name\":\"Epigenomics\",\"volume\":\" \",\"pages\":\"215-231\"},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2024-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Epigenomics\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.2217/epi-2023-0100\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/2/6 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Epigenomics","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2217/epi-2023-0100","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/2/6 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
POU2F2-mediated upregulation of lncRNA PTPRG-AS1 inhibits ferroptosis in breast cancer via miR-376c-3p/SLC7A11 axis.
Background: Triple-negative breast cancer (TNBC) is a subtype of BC with high rates of mortality. The mechanism of PTPRG-AS1 in ferroptosis of TNBC was investigated. Methods: Chromatin immunoprecipitation and dual-luciferase reporter assays were used to measure intermolecular relationships. MTT and colony formation assays detected cell viability and proliferation. Kits detected Fe2+ and reactive oxygen species levels. The role of PTPRG-AS1 in tumor growth was analyzed in vivo. Results:PTPRG-AS1 was increased in TNBC tissues and cells. PTPRG-AS1 silencing increased the reduction of glutathione and GPX4, increased Fe2+ and reactive oxygen species in erastin-treated cells and inhibited proliferation. POU2F2 transcriptionally upregulated PTPRG-AS1. PTPRG-AS1 targeted miR-376c-3p to upregulate SLC7A11. PTPRG-AS1 knockdown suppressed tumor growth in vivo. Conclusion: POU2F2 transcriptionally activates PTPRG-AS1 to modulate ferroptosis and proliferation by miR-376c-3p/SLC7A11, promoting TNBC.
期刊介绍：
Epigenomics provides the forum to address the rapidly progressing research developments in this ever-expanding field; to report on the major challenges ahead and critical advances that are propelling the science forward. The journal delivers this information in concise, at-a-glance article formats – invaluable to a time constrained community.
Substantial developments in our current knowledge and understanding of genomics and epigenetics are constantly being made, yet this field is still in its infancy. Epigenomics provides a critical overview of the latest and most significant advances as they unfold and explores their potential application in the clinical setting.
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