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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- Mucoepidermoid carcinoma (MEC), the most prevalent malignant salivary gland cancer, remains incompletely characterized at the molecular level. An integrated analytical pipeline was employed, combining differential expression analysis, weighted gene co-expression network analysis (WGCNA), resampling-based stability selection, machine learning, and cross-platform validation to identify robust diagnostic biomarkers for MEC. Two public microarray datasets (GSE169753 and GSE262344) were harmonized to form a discovery cohort of 49 samples (39 MEC and 10 normal salivary gland tissues) comprising 19,565 genes. Candidate biomarkers were identified by intersecting WGCNA hub genes with differentially expressed genes identified within the same 8,000-gene expression subset and further refined through 100 resampling iterations, retaining genes selected in at least 60% of the iterations. Elastic-net, random forest, and linear support vector machine models were trained, and the final gene signature was externally validated in an independent RNA-seq cohort (GSE282430). Eleven genes were identified: HTN3, MUCL1, GPR45, PLIN5, PAIP2B, PART1, CD109, PIP, ABCC6, CSN1S1, and KLK1. This signature demonstrated strong discrimination between MEC and normal salivary gland tissue and showed good cross-platform reproducibility in an independent RNA-seq cohort. Functional enrichment analyses revealed downregulation of pathways associated with normal sensory and secretory salivary functions in MEC. These results support the potential diagnostic utility of an 11-gene biomarker panel for MEC. - Source: PubMed
Publication date: 2026/08/22
Belmabrouk SabrineAl-Rawi Natheer HashimHadj Kacem Hassen - 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