SPIB Knockdown Inhibits the Immune Escape of Ovarian Cancer Cells by Reducing PD-L1 (CD274) Expression and Inactivating the JAK/STAT Pathway.

IF 1.1 4区医学 Q4 IMMUNOLOGY Iranian Journal of Immunology Pub Date : 2023-09-01 DOI:10.22034/iji.2023.98236.2559

Wenfei Gu, GuangTao Qi, Li Chen

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Abstract

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.

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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

背景:Spi-B转录因子(SPIB)是一种与肿瘤免疫相关的e - 26 (ETS)转录因子。目的:探讨SPIB在卵巢癌(OC)细胞中的作用及其机制。方法:分别采用菌落形成、EdU、流式细胞术和transwell检测细胞增殖、凋亡、迁移和侵袭。程序性死亡配体1 (PD-L1)和SPIB的结合位点使用JASPAR数据库预测，并使用ChIP和荧光素酶报告基因检测进行验证。结果:SPIB敲低可抑制OC细胞的增殖、迁移和侵袭，并显著促进凋亡(p)。结论:这些数据表明，SPIB敲低可通过下调PD-L1和灭活JAK/STAT通路抑制OC细胞的进展。

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来源期刊

Iranian Journal of Immunology Medicine-Immunology and Allergy

CiteScore

1.60

自引率

0.00%

发文量

审稿时长

12 weeks

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.