CD109 ELISA kit
- Known as:
- CD109 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CD109-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CD109 ELISA kit
Related genes to: CD109 ELISA kit
- Gene:
- CD109 NIH gene
- Name:
- CD109 molecule
- Previous symbol:
- -
- Synonyms:
- FLJ38569, DKFZp762L1111, CPAMD7
- Chromosome:
- 6q13
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-04
- Date modifiied:
- 2019-04-23
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- Trogocytosis, the contact-dependent exchange of membrane fragments between cells, is emerging as a critical regulator of tumor biology, yet its specific role in bladder cancer (BLCA) remains largely unexplored. In this study, we systematically characterized the trogocytosis-associated transcriptional landscape in BLCA and developed a robust prognostic framework, the Tro-score, based on five key genes (CLSTN2, CD109, KANK4, CTSE, and BCAS1). Validated across multiple independent cohorts, a high Tro-score was significantly associated with poor overall survival and a distinct immunosuppressive microenvironment characterized by the enrichment of Tregs, M2 macrophages, and myeloid-derived suppressor cells. Notably, the Tro-score served as a potent predictor of immunotherapy outcomes, with high-score patients exhibiting increased T-cell dysfunction and reduced clinical responsiveness to immune checkpoint inhibitors. Mechanistically, we pinpointed CD109 as a core molecular correlate of this immunosuppressive landscape through integrative analysis. To biologically validate these computational findings, we conducted extensive in vitro and in vivo experiments. Strikingly, in murine models receiving anti-PD-1 therapy and co-culture systems, we demonstrated that CD109 overexpression not only promotes tumor proliferation and invasion but also is associated with inhibited immune cell chemotaxis and CD8 T-cell cytotoxicity. These findings raise the hypothesis that tumor cells may exploit trogocytosis-related pathways to create a bidirectional interaction network that favors immune evasion-a concept that warrants direct experimental validation in future studies. - Source: PubMed
Publication date: 2026/08/11
Liu JinhuiHu MinghuiChen JinboZu XiongbingXiao JiatongPeng JianqiaoNie ZhenyuTong Shiyu - encodes a GPI-linked glycoprotein that acts as a signaling modulator in the TGF-β pathway. has emerged in several genome-wide association studies as linked to coronary artery disease, myocardial infarction, and angina pectoris. Heterozygous loss-of-function mutations in have also been reported in patients with congenital heart defects, suggesting potential developmental relevance, though has never been investigated in the context of cardiovascular development. We previously identified upregulation in murine atrioventricular valves undergoing myxomatous degeneration following a reduction of epicardial-derived cells. Here, we characterize expression in the murine cardiovascular system and assess its function during development using and approaches. - Source: PubMed
Publication date: 2026/06/19
Harvey Andrew BDrummond Jenna RTarolli Hannah GWolters Renélyn ADeepe Raymond NDevji InaraBarth Jeremy LMuise-Helmericks RobinRamos Paula SNorris Russell AWessels Andy - Colorectal cancer (CRC) is the third most prevalent type of cancer worldwide, with a poor survival rate at the metastatic stage. Here, we identify CD109-a negative regulator of TGFβ signaling-as a key driver of stemness and drug resistance through modulation of Wnt signaling in advanced CRC. CD109 expression strongly correlates with TGFβ levels in patient tumors and is enriched in the aggressive CRIS-B subtype, where it associates with poor clinical outcome. CD109 silencing reduced STAT3 phosphorylation and cell proliferation, without affecting migration or invasion. Moreover, global expression analysis revealed downregulation of various hallmarks of cancer stemness (i.e. LGR5 expression), together with increased TGFβ signaling and cellular senescence. Mechanistically, CD109 interacts with LRRC8A, a subunit of the volume-regulated anion channel (VRAC), which associates with AKAP12 to activate PKCα and promote STAT3 phosphorylation. This CD109/LRRC8A/AKAP12/PKCα axis sustains Wnt signaling, stemness, and drug resistance. Consistently, co-expression of CD109/LRRC8A/AKAP12 correlates with poor prognosis in CRC patients. Genetic or pharmacological disruption of this CD109/LRRC8A/AKAP12/PKCα axis impaired STAT3 signaling, reduced LGR5 expression and Wnt signaling, and sensitized cells to chemotherapy. , CD109 or LRRC8A knockdown significantly impaired liver homing and metastatic colonization in mouse models, showing stronger effects in Swiss nude mice than in highly immunodeficient NSG mice. Collectively, these findings support CD109 as a central regulator for STAT3-driven stemness and chemoresistance in advanced CRC, via the LRRC8A/AKAP12/PKCα axis, and highlight its potential value as a therapeutic target in metastatic disease. - Source: PubMed
Publication date: 2026/06/04
Bartolomé Rubén ACalvo-López TaniaOtero-Núñez PabloEstaras MaríaFernández-Barral AsunciónBarbáchano AntonioBoukich IssamCuerda-López MaríaFernández-Aceñero Mª JesúsRodríguez-Urquirizar GoraneMariscal-Casero AnaPadilla-Blanco MiguelMontoya MaríaO'Loghlen AnaFernández-Fernández José MGonzalez-Sancho Jose ManuelCasal J Ignacio - CD109 is a glycosylphosphatidylinositol‑anchored glycoprotein implicated in tumor progression and physiological homeostasis. Although aberrant CD109 expression has been reported in multiple malignancies, its prognostic relevance across cancer types and its potential immunomodulatory roles remain incompletely characterized. - Source: PubMed
Publication date: 2026/05/01
Li FangqiongZhang WeiGong XiaotingLiu DanYou QiLi YingZhao GuizhiWang Wei - The effective treatment of nasopharyngeal carcinoma (NPC) is challenged by an immunosuppressive tumor microenvironment (TME) and insufficient immune effector cell activation. Herein, we design a synergistic tri-modal therapeutic strategy to overcome these barriers. This platform integrates: (1) a CD109-targeted liposomal doxorubicin (S3-Lip-DOX) for precise chemotherapy and induction of immunogenic cell death (ICD); (2) non-genetically engineered natural killer (NK) cells armed with dual aptamers (targeting CD109 and PD-L1) bio-orthogonal chemistry for enhanced tumor recognition (S3-P-NK); and (3) an Fc-engineered anti-PD-L1 antibody (Atezolizumab/IgG1) that restores antibody-dependent cellular cytotoxicity (ADCC). Crucially, we uncovered a key mechanistic synergy: S3-Lip-DOX treatment, as a stress-adaptive response, upregulates PD-L1 expression on NPC cells. This finding provides a compelling rationale for the integration, turning a potential immune escape mechanism into a therapeutic vulnerability. The complete regimen, comprising S3-Lip-DOX, S3-P-NK, and Atezolizumab/IgG1, demonstrated potent synergistic antitumor effects and . This triple-combination therapy not only achieved significant tumor regression but also robustly reprogrammed the innate tumor microenvironment, evidenced by enhanced dendritic cell (DC) maturation and pro-inflammatory macrophage activation. This work establishes a mechanism-driven, modular therapeutic platform that effectively coordinates targeted chemotherapy with innate immunotherapy, holding significant translational potential for solid tumors. - Source: PubMed
Publication date: 2025/10/14
Yao ChaoyanWang LeiLiu WeidongShi NingLiao ZilingFu YuxuanOuyang JinhaoLei XuanHuang QianpingLi SiyuZhouyang YihuaZhao PinnanWang JieXu HongjuanZhou WenhuJiang XingjunGao XiangRen CaipingLuo Longlong