ETV7 Antibody - C-terminal (OAAB17893)
- Known as:
- ETV7 Antibody - C-terminal (OAAB17893)
- Catalog number:
- oaab17893
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ETV7 Antibody - C-terminal (OAAB17893)
Related genes to: ETV7 Antibody - C-terminal (OAAB17893)
- Gene:
- ETV7 NIH gene
- Name:
- ETS variant 7
- Previous symbol:
- -
- Synonyms:
- TEL2, TEL-2
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-19
- Date modifiied:
- 2016-10-05
Related products to: ETV7 Antibody - C-terminal (OAAB17893)
Related articles to: ETV7 Antibody - C-terminal (OAAB17893)
- Immune checkpoint blockade has improved outcomes for patients with head and neck squamous cell carcinoma (HNSCC), but reliable biomarkers for predicting therapeutic response remain limited. Tumor-reactive T-cell states are increasingly recognized as critical determinants of antitumor immunity; however, progression-associated T-cell programs that reflect tumor evolution and predict immunotherapy benefit remain insufficiently characterized. We integrated single-cell transcriptomic and T-cell receptor (TCR) sequencing data from HPV-negative HNSCC progression models to identify T-cell genes associated with tumor progression and TCR-supported immune states. Candidate genes were further refined using pretreatment immunotherapy cohorts, and a five-gene signature (HNSC-TstcSig) was established using survival and response-associated analyses. The predictive performance of HNSC-TstcSig was evaluated across multiple immunotherapy cohorts, including HNSCC and melanoma data sets. Single-cell transcriptomic analyses, spatial transcriptomic analysis, and multiplex immunofluorescence were performed to characterize the biological features of HNSC-TstcSig-associated immune states. In addition, machine learning-based survival modeling was conducted to identify genes shared between immunotherapy response and natural prognosis. HNSC-TstcSig, consisting of GBP2, HAVCR2, ETV7, ICOS, and IL2RA, showed consistent associations with immunotherapy response across multiple cohorts and reflected an immune-inflamed tumor microenvironment characterized by enhanced immune infiltration, T-cell activation, and immune checkpoint-related programs. Single-cell analyses revealed that HNSC-TstcSig genes were predominantly enriched in activated CD8 T-cell populations and were associated with cytotoxic and inflammatory immune states. Among the signature genes, ICOS showed consistent associations with CD8 T-cell activation, cytotoxicity, and immune checkpoint-related features. Network perturbation analysis further suggested that ICOS was connected with transcriptional programs involved in T-cell functional regulation. Spatial transcriptomic analysis and multiplex immunofluorescence further supported the association between ICOS-related immune features and tumor immune activity at the tissue level. Furthermore, a machine learning-derived natural prognostic model identified ICOS as a shared gene linking immunotherapy response and survival outcomes. We developed a progression-associated T-cell signature, HNSC-TstcSig, that predicts immunotherapy response and reflects immune-active tumor states in HNSCC. Our findings suggest that ICOS is associated with a tumor-reactive CD8 T-cell state characterized by cytotoxic activity and immune checkpoint-related features, providing a potential biomarker for immune stratification and a framework for understanding T-cell states associated with therapeutic benefit. - Source: PubMed
Publication date: 2026/09/27
Zhang ShaoqianYan XiaotongDong XichenAn ChangmingGu TaoWen Tao - Lumbar spinal stenosis (LSS) is commonly caused by ligamentum flavum hypertrophy (LFH), yet the underlying mechanisms remain unclear. This study investigates the role of TREM2 in macrophages during LFH pathogenesis. Immune infiltration and single-cell analyses revealed increased M2 macrophage infiltration in LFH tissues, a finding validated in a bipedal standing mouse model where macrophage depletion attenuated fibrosis. In vitro, M2 macrophages promoted fibrosis in human ligamentum flavum cells in a TREM2-dependent manner. Mechanistically, TREM2 suppressed the transcription factor ETV7, which binds the TGF-β1 promoter to inhibit its transcription, while simultaneously activating the PI3K/Akt/HIF-2α axis to enhance TGF-β1 expression. TGF-β1 then activated Smad2/3 signalling via ALK5, driving fibrotic gene expression. Additionally, Galectin-3, which was markedly upregulated in LFH tissues, facilitated the activation of TREM2. TREM2 knockout mice exhibited reduced LFH, confirming in vivo relevance. Collectively, these findings demonstrate that TREM2 in M2 macrophages promotes LFH by relieving ETV7-mediated repression and activating the PI3K/Akt/HIF-2α/TGF-β1 cascade, positioning TREM2 as a potential therapeutic target for LSS. - Source: PubMed
Publication date: 2026/08/16
Qiu JieChen TongZhang YihanGe YaningGao TianshuZhang HelongLv SongtaoWang ZhengboJiang TaoMa ChengRen Yongxin - The present study aimed to characterize the immune response, differential gene expression, and functional alterations observed following an in vivo challenge of Classical Swine Fever Virus (CSFV) in crossbred pigs. RNA-sequencing was performed on whole blood samples collected from three pigs before and at 7 days post-infection. A total of 3428 differentially expressed genes (DEGs) were identified, including 970 significantly upregulated and 261 downregulated genes (|log fold change| ≥ 1.5, adjusted p < 0.05). The most prominent DEG was LAMB4, a gene associated with cellular attachment receptors facilitating CSFV binding to porcine cells. Several cytokine-cytokine receptor interaction genes, such as CXCL12, CCL2, CCR1, and IL10RA, were upregulated, indicating a strong activation of innate immune responses. Simultaneously, multiple adaptive immune genes, including CD28, CD83, SLA-DQB1, and IL1A, IL12A, IL26 were downregulated, suggesting viral-mediated suppression of antigen presentation and T-cell signaling. Pathway analysis highlighted the involvement of platelet activation and coagulation cascades during viral evasion. Protein-protein interaction (PPI) analysis revealed a core antiviral module comprising MX1, MX2, ISG15, IFIH1, OASL, IFIT1, and UBE2L6, which are central to interferon signaling and viral restriction. Transcription factors such as ETV7, TOX3, and MSC were upregulated, pointing to immune modulation and possible T-cell exhaustion. Conversely, downregulation of HES1, PRDM6, and MYOG indicated impaired lymphocyte differentiation and tissue repair. Overall, the findings suggest a dual host response to CSFV, with strong innate activation alongside adaptive immune suppression, providing valuable insights for vaccine and therapeutic development. - Source: PubMed
Publication date: 2026/06/25
Singh AyushiKumar AmitKhanna ShivaniDhar PronabLatheef Shyma KUpmanyu VikramadityaAgrawal Ravi KantYadav Ajay KumarUpadhyay AmritanshuChand Devatwal PremDwivedi ShraddhaDutt Triveni - The immunosuppressive tumor microenvironment (TME) serves as a central driver of bladder cancer (BCa) progression and prognosis. While its significance is widely acknowledged, the key cellular subsets that mediate this immunosuppressive state and their core regulatory genes remain incompletely understood. Key immunosuppressive cellular subsets and their signature genes were systematically identified using single-cell RNA sequencing (scRNA-seq) data from BCa samples. A prognostic risk model was then constructed via univariate and multivariate Cox regression analyses, based on bulk RNA-seq datasets and the identified signature genes. The role of SUSD2 was further validated in vitro using qRT-PCR, Western blot, immunofluorescence, proliferation, and invasion assays. Compared with adjacent normal tissues, BCa tissues showed significant enrichment of stromal cells (e.g., epithelial cells, fibroblasts). Among these stromal populations, the proportion of myofibroblast-like cancer-associated fibroblasts (myCAFs) was significantly increased in BCa tissues, and high myCAF infiltration was closely associated with poor patient prognosis. Pseudotime trajectory analysis confirmed that fibroblast differentiation in BCa shifts toward a terminal state (State 3), which is predominantly composed of myCAFs. A prognostic model established using myCAF-related signature genes (TMEM74B, ABCC9, FCMR, ALG9, SUSD2, and ETV7) exhibited stable predictive performance in both training and validation cohorts, with SUSD2 identified as a risk-related gene. In vitro experiments revealed that SUSD2 knockdown inhibited myCAF activation and extracellular matrix secretion, thereby attenuating its promotional effects on BCa cell proliferation and invasion. The TGF-β receptor inhibitor SB-431542could reverse the facilitative effects of SUSD2 overexpression on tumor cell proliferation and migration. Our findings identify myCAFs as a core regulatory cellular subset and SUSD2 as a key molecule within the immunosuppressive TME of BCa. Additionally, SUSD2 may trigger the activation of the TGF-β/Smad signaling cascade to induce myCAF activation, thereby accelerating BCa progression. These results provide novel potential targets and a theoretical basis for prognosis assessment and TME-targeted therapy in BCa. - Source: PubMed
Publication date: 2026/06/19
Song WeihangHan GuangyeLi ZhenhuiHu JunlingMa Kuo - Resistance to 5-fluorouracil (5-FU) remains a major challenge in the treatment of colorectal cancer (CRC). Here, we identify ETS variant transcription factor 7 (ETV7) as significantly upregulated in CRC tissues and cell lines, with elevated expression associated with poor clinical prognosis. Functional assays demonstrate that ETV7 enhances CRC cell proliferation, invasion, and resistance to 5-FU. Mechanistically, ETV7 transcriptionally upregulates CXCL1, leading to increased neutrophil recruitment and enhanced formation of neutrophil extracellular traps (NETs). The resulting NETs-enriched tumor microenvironment promotes tumor aggressiveness and chemoresistance. Pharmacological inhibition of CXCL1 or degradation of NETs effectively attenuates ETV7-driven malignant phenotypes in vitro and in vivo. Collectively, these findings establish an ETV7-CXCL1-NETs axis that contributes to 5-FU resistance in CRC and suggest that targeting this pathway may improve chemotherapy response. - Source: PubMed
Publication date: 2026/03/31
Mo ShuangXia PeiLv YongruiLiu LeiHe ShujinGao HuabinChen LinWu JianqiangHan AnjiaChen Lixia