Characterization of immune landscape and prognostic value of IL-17-related signature in invasive breast cancer.

IF 1.5 4区 医学 Q4 ONCOLOGY
Translational cancer research Pub Date : 2025-02-28 Epub Date: 2025-02-26 DOI:10.21037/tcr-24-1632
Wenge Dong, Xiaojie Gu, Jiejing Li, Zhigang Zhuang
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引用次数: 0

Abstract

Background: Recently, interleukin 17 (IL-17) has been found to play a critical role in the development of breast cancer. However, its prognostic significance in invasive breast cancer (IBC) remains unclear. This study aims to determine the role of IL-17-related signatures in IBC to identify novel therapeutic options.

Methods: IBC data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) were used to identify IL-17-related prognostic genes. A predictive model was developed using TCGA data and validated using METABRIC data. The relationship between IL-17 scores and immune landscape, chemotherapy drug sensitivity [half maximal inhibitory concentration (IC50)], and immune checkpoint gene expression was analyzed. The quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to validate key gene expression in breast tumor and normal tissue samples.

Results: The predictive model identified core IL-17-related prognostic genes and successfully estimated the prognosis of IBC patients. The model's validity was confirmed using METABRIC data. Patients with high IL-17 scores had worse overall survival (OS) compared to those with low IL-17 scores. Low IL-17 scores were associated with higher immune checkpoint gene expression and predicted enhanced responses to cytotoxic T-lymphocyte-associated protein 4 (CTLA4) and programmed cell death protein 1 (PD-1) therapies. Patients with low IL-17 scores exhibited a higher abundance of immune microenvironment components. Furthermore, qRT-PCR confirmed the lower expression of OR51E1, NDRG2, RGS2, and TSPAN7 in breast tumors compared to normal tissue.

Conclusions: IL-17-related signatures are promising biomarkers for predicting the prognosis of IBC patients. These findings suggest that IL-17-related markers could be used to guide individualized therapeutic strategies, potentially improving outcomes for IBC patients.

浸润性乳腺癌免疫景观特征及il -17相关特征的预后价值
背景:近年来,人们发现白细胞介素17 (IL-17)在乳腺癌的发展中起着至关重要的作用。然而,其在浸润性乳腺癌(IBC)中的预后意义尚不清楚。本研究旨在确定il -17相关特征在IBC中的作用,以确定新的治疗方案。方法:使用来自癌症基因组图谱(TCGA)、基因表达图谱(GEO)和乳腺癌国际分子分类协会(METABRIC)的IBC数据鉴定il -17相关预后基因。使用TCGA数据建立预测模型,并使用METABRIC数据进行验证。分析IL-17评分与免疫景观、化疗药物敏感性[半数最大抑制浓度(IC50)]、免疫检查点基因表达的关系。采用定量反转录聚合酶链反应(qRT-PCR)验证关键基因在乳腺肿瘤和正常组织样本中的表达。结果:该预测模型识别了核心il -17相关预后基因,成功预测了IBC患者的预后。利用METABRIC数据验证了模型的有效性。与低IL-17评分的患者相比,高IL-17评分的患者总生存期(OS)更差。低IL-17评分与较高的免疫检查点基因表达相关,并预测对细胞毒性t淋巴细胞相关蛋白4 (CTLA4)和程序性细胞死亡蛋白1 (PD-1)治疗的反应增强。IL-17评分低的患者表现出更高的免疫微环境成分丰度。此外,qRT-PCR证实OR51E1、NDRG2、RGS2和TSPAN7在乳腺肿瘤组织中的表达低于正常组织。结论:il -17相关特征是预测IBC患者预后的有希望的生物标志物。这些发现表明,il -17相关标志物可用于指导个体化治疗策略,潜在地改善IBC患者的预后。
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来源期刊
CiteScore
2.10
自引率
0.00%
发文量
252
期刊介绍: Translational Cancer Research (Transl Cancer Res TCR; Print ISSN: 2218-676X; Online ISSN 2219-6803; http://tcr.amegroups.com/) is an Open Access, peer-reviewed journal, indexed in Science Citation Index Expanded (SCIE). TCR publishes laboratory studies of novel therapeutic interventions as well as clinical trials which evaluate new treatment paradigms for cancer; results of novel research investigations which bridge the laboratory and clinical settings including risk assessment, cellular and molecular characterization, prevention, detection, diagnosis and treatment of human cancers with the overall goal of improving the clinical care of cancer patients. The focus of TCR is original, peer-reviewed, science-based research that successfully advances clinical medicine toward the goal of improving patients'' quality of life. The editors and an international advisory group of scientists and clinician-scientists as well as other experts will hold TCR articles to the high-quality standards. We accept Original Articles as well as Review Articles, Editorials and Brief Articles.
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