PLXDC1 Antibody (OASA08849)
- Known as:
- PLXDC1 Antibody (OASA08849)
- Catalog number:
- oasa08849
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PLXDC1 Antibody (OASA08849)
Related genes to: PLXDC1 Antibody (OASA08849)
- Gene:
- PLXDC1 NIH gene
- Name:
- plexin domain containing 1
- Previous symbol:
- -
- Synonyms:
- TEM3, TEM7
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-08-27
- Date modifiied:
- 2016-10-05
Related products to: PLXDC1 Antibody (OASA08849)
Related articles to: PLXDC1 Antibody (OASA08849)
- The 5-year overall survival rate for hepatocellular carcinoma (HCC) patients remains below 20%. Alterations in the extracellular matrix (ECM) are increasingly recognized as central drivers of HCC initiation and progression. This study applied a system biology framework integrating omics data and machine learning to analyze gene expression and regulatory networks in HCC using The Cancer Genome Atlas. Eight ECM-associated genes (, , , , , , , and ) were identified as upregulated diagnostic biomarkers with strong discriminatory power. Among them, , , and showed significant associations with poor overall survival, defining a prognostic subset. Validation in the GSE104310 and GSE144269 datasets confirmed consistent expression patterns across cohorts. Functional enrichment linked these genes to tissue remodeling and angiogenesis. Single-cell RNA sequencing revealed upregulation in T cells, enrichment in cancer-associated fibroblasts, and mild elevation in tumor-associated macrophages and endothelial cells. These findings identify key ECM-based biomarkers with potential for early detection, prognosis, and therapeutic targeting in HCC. - Source: PubMed
Publication date: 2026/02/24
Sarabi Pedram AsadiRismani ElhamJudaki Amir AliFarrokhzad AmirhosseinHendi ZahraHassan MoustaphaVosough Massoud - BACKGROUND: While single-cell technologies have advanced bladder cancer research, the microenvironment of lymph node metastases and its role in progression remain unclear. We aimed to elucidate dynamic tumor-microenvironment interactions across metastatic and primary sites, identify poor-prognosis features, and uncover novel therapeutic targets. METHODS: We profiled matched single-cell and spatial transcriptomic samples from lymph node-metastasized bladder cancer to construct a high-resolution atlas. Bioinformatic analyses were used to inferred ligand-receptor interactions, regulatory networks, and spatial co-localization. Integration with multiple prognostic cohorts revealed key cell subpopulations linked to tumor biology and poor outcomes. RESULTS: Our atlas included 32 samples, 61 cell subtypes, key ligand signals (e.g., TGFB1, OSM, IFNG), 343 transcription factors, 188 co-localization events, over 1,000 spatially validated interactions, and 21 cell niches. Tumor-driven convergence was observed across distinct microenvironments. Notably, a pericyte-like myofibroblast subtype, myoCAF_PLXDC1, was enriched in malignant tissues, associated with poor prognosis, and exhibited enhanced angiogenic but reduced chemotactic activity compared to myoCAF_CCL21. Its phenotype was linked to intracellular regulators (PRRX1 and MXD4) and extracellular signals (IFNG and TGFB1). Spatially, myoCAF_PLXDC1 co-localized with ITGA8+ endothelial cells and enriched in tumor regions. CONCLUSIONS: This study offers a comprehensive resource for lymph node-metastasized bladder cancer and identifies PLXDC1+ fibroblasts co-localized with ITGA8+ ECs as potential components of a tumor-specific vascular niche and therapeutic target. - Source: PubMed
Publication date: 2025/12/15
Wang ZiweiMiao JiayingWang MaoyuYing YidieZhang ZhenshengZeng ShuxiongXu Chuanliang - The damage of ferroptosis is related to the pathogenesis of intervertebral disc degeneration (IDD). N6-methyladenosine (m6A) modification accounts for more than 80% of RNA modifications in eukaryotic cells. However, the key role of m6A related ferroptosis-related genes (FRGs) in IDD remain explorable. Firstly, batch correction between datasets was performed. Weighted gene co-expression network analysis (WGCNA) was then conducted to acquire the most relevant module genes. Differentially expressed genes (DEGs) between the IDD and Normal Group were obtained by differential analysis subsequently. Next, according to the Pearson correlation and the intersection of m6A and FRGs related genes, m6A-FRGs related genes were selected. Additionally, we intersected module genes, DEGs and m6A-FRGs related genes to obtain DEGs of m6A-FRGs related module genes (m6A-FRGs-DEGs). Least absolute shrinkage and selection operator (LASSO) was applied to get HUBgenes. After, we conducted gene set enrichment analysis (GSEA) to gain function items and related pathways of HUBgenes. Single sample gene set enrichment analysis (ssGSEA) and wilcox.test were proceeded to analyse differences in relative abundance of immune cells between the IDD and Normal Groups, and a nomogram was constructed based on significantly different HUBgenes. The Comparative Toxicogenomics Database (CTDbase) was then applied to predict potential drugs or molecular compounds that could modulate HUBgenes. Last but not least, we performed the quantitative real-time fluorescence PCR (qRT-PCR) to verify HUBgenes. 181 m6A-FRGs-DEGs were acquired by the intersection of key module genes (from MEtan, MEsalmon, MEbrown and MEgreen), 362 DEGs and 15,678 m6A-FRGs related genes. Subsequent analysis showed that HUBgenes (ZNF595, PLXDC1, FNBP1L, KLRB1, NRCAM, PPCDC, C9orf139, SIGLEC17P, RRAS2 and DPRXP4) significantly participated in positive regulation of cytokine production, mitochondrial inner membrane and organellar ribosome. Besides, the relative abundance of neutrophils was found significantly different between IDD and normal groups. A nomogram was constructed based on ZNF595 and RRAS2, and there were 11 drugs targeted on ZNF595, while 118 drugs predicted based on RRAS2 such as Tetrachlorodibenzodioxin, Bisphenol A and Benzo(a)pyrene. Lastly, ZNF595 and RRAS2 were both obviously up-regulated in IDD according to the qRT-PCR. Our research suggested 10 HUBgenes were significantly associated with IDD, providing more evidence about the vital role of HUBgenes in IDD. - Source: PubMed
Publication date: 2025/09/29
Che ZhenChen RuibingLi MingLiao ZhuangyaoWang KunYao DengboLiang YuweiLi YuxiWen GuomingXing TongSu KaihuiLiang ChangchunHuang LinZhao Qun - Pancreatic stellate cells (PSCs) contribute to pancreatic ductal adenocarcinoma (PDAC) progression and therapeutic resistance, yet their detailed functions remain unclear. This study combined RNA sequencing and assay for transposase-accessible chromatin using sequencing (ATAC-seq) on sorted PSCs from adjacent normal and PDAC tissues to investigate their transcriptional and epigenetic activation. PSCs heterogeneity and functions are characterized through bulk, single-cell, and spatial transcriptomes, as well as in situ sequencing. The clinical relevance of PSCs in immunotherapy is assessed using an in-house immune-checkpoint blockade (ICB) treatment cohort. Findings showed that stress and hypoxia signaling activated PSCs in PDAC. Three common PSCs (CPSCs) and four tumor-associated PSCs (TPSCs) are identified, each with distinct functions. CPSCs differentiated into CCL19 TPSCs in immune-enriched regions, MYH11 TPSCs in the stromal region, and PLXDC1 TPSCs, which exhibited cancer-associated myofibroblasts (myCAFs) phenotype linked to poor prognosis. Notably, PLXDC1 TPSCs, located near aggressive LRRC15 myCAFs and SPP1 macrophages, formed a desmoplastic and immunosuppressive niche around the tumor boundary, promoting CD8 T cell exhaustion. Single-cell transcriptomics of PDAC patients treated with ICB revealed that PLXDC1 TPSCs correlated with poor immunotherapy efficacy. Overall, this study provides key insights into PSCs in PDAC and potential therapeutic targets. - Source: PubMed
Publication date: 2025/03/17
Du YanhuaZhao YizhouLi JudongWang JiaxinYou ShenglanZhang YaoZhang LiYang JihongAlinejad-Rokny HamidCheng ShujieShao ChenghaoZou DuowuYe Youqiong - Rare earth is used extensively around the world, and rare earth particles cause a respiratory disease in workers termed rare earth pneumoconiosis(REP) that have attracted considerable attention. However, the mechanisms of REP, characterized by diffuse pulmonary fibrosis, are elusive. REP progression involves various signaling pathway networks comprising numerous cell types and cytokines. Acting as an important medium for communication between cells, exosomes are emerging as a major research topic. However, the role of exosomal lncRNAs, miRNAs and mRNAs in REP remains unclear. In the present study, we conducted high-throughput RNA sequencing to generate long non-coding RNA(lncRNA), microRNA (miRNA) and mRNA profiles from the serum exosomes of nine patients with rare earth pneumoconiosis and nine healthy people. Our results identified a total of 94 lncRNAs, 93miRNAs, and 29 mRNAs were differentially expressed in the serum exosomes of patients with rare earth pneumoconiosis. Subsequently, Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to analyze the differentially expressed RNAs. The abundant enriched GO terms of exosomal genes are cytoplasm, protein binding, cytoskeleton, Nuclear cytoplasmic transport, and KEGG pathways of exosomal genes included metabolic and cancer pathway, PI3K/Akt, wnt, mTOR, HIF-1, actin cytoskeleton and cell cycle and so on. RT-qPCR results showed that lnc-KCNMB2-AS1, hsa-miR-186-5p, hsa-miR-100-5p, hsa-miR-381-5p, NCOA4 and PLXDC1 were up-regulated, and lnc-TMEM151A, hsa-miR-758-5p and hsa-miR-6842-5p were significantly down-regulated in exosomes. In addition, our study fuond that the PI3K/Akt pathway was activated, and the expression level of miR-100-5p was increased synchronously in lung tissue of mice exposed to rare earth NdO. In this study, PI3K/Akt pathway is significant helpful in elucidating the mechanism of REP. These findings can provide new insights into the mechanism of REP and develop a novel treatment strategy and biomarker. - Source: PubMed
Publication date: 2025/01/03
Gao YanrongWang ShuruiHe YuanqiMa YupengWang Suhua