TSPAN8 Antibody
- Known as:
- TSPAN8 Antibody
- Catalog number:
- XW-8169
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- TSPAN8 Antibody
Related genes to: TSPAN8 Antibody
- Gene:
- TSPAN8 NIH gene
- Name:
- tetraspanin 8
- Previous symbol:
- TM4SF3
- Synonyms:
- CO-029
- Chromosome:
- 12q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-16
- Date modifiied:
- 2016-01-15
Related products to: TSPAN8 Antibody
Related articles to: TSPAN8 Antibody
- Tumor cells evade anti-tumor immunity by reprogramming tumor microenvironment (TME). Using multiplexed single-cell proteomics to analyze 50 TME-associated proteins across treatment-naive triple-negative breast cancer (TNBC) specimens, we discovered that cancer stem cells (CSCs) drive differentiation and expansion of regulatory T cells (Tregs) via extracellular vesicle (EV)-mediated paracrine signaling. TSPAN8, an integral membrane protein on CSC-derived EVs, interacts with CD103 (integrin αEβ7) on T cells, triggering the formation of LKB1-STRAD-MO25 complex and sequential phosphorylation of LKB1 and AMPKα. This cascade enhances FOXP3 expression, which transactivates CD103, creating a positive feedback loop that drives clonal expansion of immunosuppressive CD103FOXP3 Tregs and their associated niche. This EV membrane topology-based mechanism operates independently of canonical EV cargo internalization. Neutralizing EVs-TSPAN8 with a monoclonal antibody synergized with anti-PD-1 therapy in preclinical models, suggesting a potential approach targeting both CSCs and TME immunosuppression, particularly in TNBC subpopulation with high TSPAN8 CSCs. - Source: PubMed
Publication date: 2026/05/07
Fan GuangjianJin JuanWang JieXu JingxuanGe WeiyuLiu SulingTang LeiReziya WumaierYang XiaoyiLi JunjianNg Lai GuanDi LijunZheng YuantingLan FeiChen ShizhuoZhang YanWang XinGao DongLiu XindongSun HaoyuLiu YinbingLi TingCao YiqunTao ZhonghuaLiu WentingWang Hongxia - Acquired radioresistance remains a major obstacle to effective radiotherapy for cervical cancer, often driven by epithelial-mesenchymal transition (EMT). This study reveals TSPAN8 as a novel regulator of EMT-mediated radioresistance, offering new insights for overcoming treatment failure. Radioresistant subclones of HeLa-R25 and SiHa-R25 cells were established by repeated 2 Gy fractions. Radioresistance, apoptosis, EMT, and stemness were assessed by clonogenic survival, flow cytometry, immunoblotting, and immunofluorescence. Differentially expressed genes were identified by microarray, validated by protein-protein interaction analysis and co-immunoprecipitation, and functionally examined via TSPAN8 overexpression/knockdown, xenograft models, and immunohistochemistry of primary, metastatic, and recurrent post-radiotherapy specimens. Prognostic relevance was analyzed in the TCGA-CESC cohort. Fractionated irradiation induced EMT and radioresistance, with significantly higher clonogenic survival in R25 cells (P < 0.05), characterized by E-cadherin loss, N-cadherin/Vimentin upregulation, and increased CD44/Oct4. TSPAN8 was the most upregulated gene and directly interacted with E-cadherin. Overexpression enhanced EMT, invasion, and resistance to apoptosis, while knockdown reversed these effects and restored radiosensitivity in vivo. TSPAN8 knockdown in radioresistant xenografts significantly suppressed tumor growth (P < 0.05), and combined knockdown with irradiation further reduced tumor volume (P < 0.05). In patient samples, post-radiotherapy recurrences and metastases exhibited high TSPAN8 and vimentin with reduced E-cadherin. TCGA data confirmed that elevated TSPAN8 was associated with worse outcomes, including shorter disease-specific survival (HR = 2.02, 95% CI 1.01-3.71, P = 0.02) and progression-free survival (HR = 3.09, 95% CI 1.80-5.30, P < 0.001). These data suggest that TSPAN8 drives EMT-mediated radioresistance in cervical cancer, is associated with recurrence and poor survival, and represents a potential biomarker and therapeutic target. Targeting TSPAN8 may enhance radiosensitivity and improve personalized radiotherapy outcomes. - Source: PubMed
Publication date: 2026/03/27
Wang Jing-NanLiao Ling-LiYang FanWang RuZhang LeiLi Ao-XueYu Peng-JieWu Ruo-TongChen NuoXu Yu-QiaoZhou Yong-Chun - The extracellular matrix (ECM) plays a critical role in the tumor microenvironment (TME). However, the prognostic relevance of matrisome-related genes (MRGs) in bladder cancer (BLCA) remains poorly understood. This study aimed to establish a matrisome-related gene signature for prognostic stratification in bladder cancer and to further characterize its associations with tumor microenvironmental features and candidate compounds. - Source: PubMed
Publication date: 2026/04/20
Wu GongpingYu WeitaoYao DongnuanMa XuemingFan ChengweiHou JuanjuanRen XuezhaoTian Junqiang - KCNJ5-mutant aldosterone-producing adenomas (APAs) represent a primary cause of primary aldosteronism, leading to severe secondary hypertension. However, the adrenal cellular heterogeneity and microenvironmental landscape of KCNJ5-mutant APAs remain to be characterized. Using single-cell RNA sequencing and spatial transcriptomics, we analyzed three paired KCNJ5-mutant APAs and distal adrenal tissues (DATs), with experimental validation by immunohistochemistry and immunofluorescence. In DATs, we identified a previously unrecognized TSPAN8-positive zona glomerulosa (ZG) cell population. Pseudotime and functional enrichment analyses indicate that these cells represent an intermediate state between ZG and zona fasciculata (ZF). Within APAs, adrenocortical cells exhibited remarkable heterogeneity. The key enzyme mediating aldosterone synthesis, CYP11B2, was predominantly expressed in ZF-like cells, suggesting that targeting ZF-like cells may be critical for controlling aldosterone overproduction in APAs. Furthermore, CYP11B2-positive cells displayed two distinct functional states: Fate 1 (aldosterone-producing cells) specialized in mitochondrial metabolism and steroid hormone synthesis, while Fate 2 (tumor growth-promoting cells) participated in anti-apoptotic pathways that may drive APA cell accumulation. In contrast, CYP11B2-negative tumor cells demonstrated enhanced proliferative and differentiation potential, potentially playing a more active role in APA tumorigenesis. Notably, we discovered a unique subset of APA-associated macrophages (AAMs) within the tumor microenvironment. These AAMs were immunosuppressive and communicated with APA cells via the SPP1-(ITGAV/ITGB1) axis, likely promoting tumor proliferation. These findings provide novel insights into the cellular complexity of KCNJ5-mutant APAs, highlighting adrenal cortical cell plasticity and tumor-associated macrophages as critical determinants of APA pathogenesis. - Source: PubMed
Publication date: 2026/02/25
He FurongHu JinboZeng QinglianWang XiaoLi HongjiLi RuolinLi JiayuLi JunlongXiong YunjieYin JuanLiu YunyanPeng ChuanSong YingXu YongHuang WeiLi QifuMa LinqiangYang Shumin - Cancer-associated fibroblasts (CAFs) are a key cellular component of the tumor microenvironment (TME), which comprises distinct subtypes, each exhibiting unique and significant roles in cancer development. Senescent cancer-associated fibroblasts (senCAFs) are a newly identified subset of CAFs characterized by high expression of senescence-associated markers. Notably, senCAFs significantly promote tumor malignancy through the secretion of diverse senescence-associated secretory phenotype (SASP) factors, such as interleukin-6 (IL-6), interleukin-8 (IL-8), matrix metalloproteinases (MMPs), and transforming growth factor-β (TGF-β), thereby facilitating tumor cell proliferation, invasion, angiogenesis, immunosuppression, and resistance to cancer therapy. Consequently, targeting senCAFs-either through selective clearance of this cell subset or suppression of their SASP-represents a promising approach for cancer treatment. Emerging therapies include pharmacological inhibition of key SASP regulatory pathways (e.g., JAK/STAT3 and NF-κB) and antagonists targeting individual SASP components. Additionally, senolytic agents and therapies targeting senCAF-specific markers (e.g., TSPAN8) are being actively explored. Furthermore, immunotherapies, including CAR-T cells targeting senescence-associated surface proteins, provide intriguing avenues. These advances highlight senCAFs as attractive therapeutic targets and underscore the potential for integrating SASP inhibitors and senolytic agents into precision oncology paradigms. - Source: PubMed
Publication date: 2026/01/21
Feng YingyingZhi XiaochenXiao TingFeng Lin