{"title":"SPIB敲低通过降低PD-L1 (CD274)表达和灭活JAK/STAT通路抑制卵巢癌细胞的免疫逃逸","authors":"Wenfei Gu, GuangTao Qi, Li Chen","doi":"10.22034/iji.2023.98236.2559","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Spi-B transcription factor (SPIB) is an E-twenty-six (ETS) transcription factor associated with tumor immunity.</p><p><strong>Objective: </strong>To investigate the functions and mechanisms of SPIB in ovarian cancer (OC) cells.</p><p><strong>Methods: </strong>Cell proliferation, apoptosis, migration, and invasion were determined using colony formation, EdU, flow cytometry, and transwell assays, respectively. The binding sites of programmed death-ligand 1 (PD-L1) and SPIB were predicted using the JASPAR database and verified using the ChIP and luciferase reporter assays.</p><p><strong>Results: </strong>SPIB knockdown inhibited OC cell proliferation, migration, and invasion, and significantly boosted apoptosis (p<0.05). SPIB directly enhanced PD-L1 transcription in OVCAR-3 and SKOV3 cells (p<0.05). Importantly, the JAK/STAT pathway was markedly inactivated in OC cells upon SPIB knockdown. SPIB knockdown markedly decreased JAK2 and STAT1 phosphorylation in OVCAR-3 and SKOV3 cells (p<0.05).</p><p><strong>Conclusion: </strong>These data indicate that SPIB knockdown inhibits OC cell progression by downregulating PD-L1 and inactivating the JAK/STAT pathway.</p>","PeriodicalId":54921,"journal":{"name":"Iranian Journal of Immunology","volume":null,"pages":null},"PeriodicalIF":1.1000,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"SPIB Knockdown Inhibits the Immune Escape of Ovarian Cancer Cells by Reducing PD-L1 (CD274) Expression and Inactivating the JAK/STAT Pathway.\",\"authors\":\"Wenfei Gu, GuangTao Qi, Li Chen\",\"doi\":\"10.22034/iji.2023.98236.2559\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Spi-B transcription factor (SPIB) is an E-twenty-six (ETS) transcription factor associated with tumor immunity.</p><p><strong>Objective: </strong>To investigate the functions and mechanisms of SPIB in ovarian cancer (OC) cells.</p><p><strong>Methods: </strong>Cell proliferation, apoptosis, migration, and invasion were determined using colony formation, EdU, flow cytometry, and transwell assays, respectively. The binding sites of programmed death-ligand 1 (PD-L1) and SPIB were predicted using the JASPAR database and verified using the ChIP and luciferase reporter assays.</p><p><strong>Results: </strong>SPIB knockdown inhibited OC cell proliferation, migration, and invasion, and significantly boosted apoptosis (p<0.05). SPIB directly enhanced PD-L1 transcription in OVCAR-3 and SKOV3 cells (p<0.05). Importantly, the JAK/STAT pathway was markedly inactivated in OC cells upon SPIB knockdown. SPIB knockdown markedly decreased JAK2 and STAT1 phosphorylation in OVCAR-3 and SKOV3 cells (p<0.05).</p><p><strong>Conclusion: </strong>These data indicate that SPIB knockdown inhibits OC cell progression by downregulating PD-L1 and inactivating the JAK/STAT pathway.</p>\",\"PeriodicalId\":54921,\"journal\":{\"name\":\"Iranian Journal of Immunology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.1000,\"publicationDate\":\"2023-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Iranian Journal of Immunology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.22034/iji.2023.98236.2559\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Iranian Journal of Immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.22034/iji.2023.98236.2559","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
SPIB Knockdown Inhibits the Immune Escape of Ovarian Cancer Cells by Reducing PD-L1 (CD274) Expression and Inactivating the JAK/STAT Pathway.
Background: Spi-B transcription factor (SPIB) is an E-twenty-six (ETS) transcription factor associated with tumor immunity.
Objective: To investigate the functions and mechanisms of SPIB in ovarian cancer (OC) cells.
Methods: Cell proliferation, apoptosis, migration, and invasion were determined using colony formation, EdU, flow cytometry, and transwell assays, respectively. The binding sites of programmed death-ligand 1 (PD-L1) and SPIB were predicted using the JASPAR database and verified using the ChIP and luciferase reporter assays.
Results: SPIB knockdown inhibited OC cell proliferation, migration, and invasion, and significantly boosted apoptosis (p<0.05). SPIB directly enhanced PD-L1 transcription in OVCAR-3 and SKOV3 cells (p<0.05). Importantly, the JAK/STAT pathway was markedly inactivated in OC cells upon SPIB knockdown. SPIB knockdown markedly decreased JAK2 and STAT1 phosphorylation in OVCAR-3 and SKOV3 cells (p<0.05).
Conclusion: These data indicate that SPIB knockdown inhibits OC cell progression by downregulating PD-L1 and inactivating the JAK/STAT pathway.
期刊介绍：
The Iranian Journal of Immunology (I.J.I) is an internationally disseminated peer-reviewed publication and publishes a broad range of experimental and theoretical studies concerned with all aspects of immunology.
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