APMAP ELISA kit
- Known as:
- APMAP Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-APMAP-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- APMAP ELISA kit
Related genes to: APMAP ELISA kit
- Gene:
- APMAP NIH gene
- Name:
- adipocyte plasma membrane associated protein
- Previous symbol:
- C20orf3
- Synonyms:
- BSCv
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-19
- Date modifiied:
- 2016-10-05
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- Multiple primary cancers (MPC) refer to the occurrence of two or more independent primary malignant tumors in the same patient, either simultaneously or metachronously. Their clinical diagnosis and differential diagnosis are challenging, treatment strategies are complex, and the incidence has been increasing in recent years. However, there is still a lack of potential biomarkers that can be used for early identification and prognosis assessment, which has become a key bottleneck in current research. This study employed Oxford Nanopore Technologies (ONT) long-read transcriptome sequencing and data-independent acquisition (DIA) proteomics to perform integrated multi-omics analysis of blood samples from patients with only primary lung cancer (OPLC), lung cancer with MPC, and healthy controls (HC), systematically characterizing the molecular features of MPC at both transcript and protein levels. The results showed that MPC patients exhibited significantly increased transcript complexity, with the numbers of differentially expressed genes (DEGs), differentially expressed transcripts (DETs), and differential transcript usage (DTU) events being substantially higher than those in OPLC and HC groups. Multiple genes displayed rich isoform diversity. Functional enrichment analysis indicated that MPC-specific molecules were significantly enriched in immune- and inflammation-related pathways such as NF-κB, NOD-like receptor, Toll-like receptor, and TNF signaling. By integrating gene, transcript, and protein expression profiles, several core molecules (e.g., ATP6AP2, APMAP, CIAO2A, and ITGB2) with consistent expression across multiple regulatory levels were identified, all showing significant and consistent alterations in MPC. This study reveals the molecular characteristics of transcript isoform complexity in the blood samples of MPC patients through long-read sequencing combined with proteomics, providing important theoretical insights for understanding the mechanisms of MPC and identifying potential targets. - Source: PubMed
Publication date: 2026/02/27
Huang YingkuiZhu GuangzhiYang HuanjuanZhang YanfeiTian HongwuCao JingLi ShengmeiLiu GuoweiMa Husai - Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related deaths worldwide. Adipocyte Plasma Membrane Associated Protein (APMAP) is a glycosylated type II transmembrane protein, and APMAP induces malignant metastasis of colorectal cancer. However, the role and mechanism of APMAP in NSCLC remain unknown. We aimed to study the APMAP regulation on NSCLC. APMAP mRNA levels in NSCLC tissues were tested by quantitative reverse transcription-PCR (qRT-PCR). APMAP protein levels in NSCLC tissues and cells were determined via Western blot. Also, the association between APMAP expressions and NSCLC clinicopathology was assessed using Chi-square test. After silencing APMAP (sh-APMAP) in NSCLC cells, APMAP's roles in NSCLC were revealed by Western blot, Cell Counting Kit-8 (CCK-8) assay, Transwell, Fe level analysis, and immunofluorescence assays. Meanwhile, APMAP mechanism in NSCLC was verified through Human TFDB and PROMO databases, qRT-PCR, Western blot, dual-luciferase reporter assay, CCK-8 experiment, Transwell, analysis of Fe, reactive oxygen species levels, and Clinical Bioinformatics Home. Also, APMAP function in vivo was examined using a tumor xenograft model, immunohistochemistry assay, and Western blot. APMAP expressions were up-regulated in NSCLC tissues and cells. Moreover, patients with high APMAP expression exhibited a poorer overall survival rate. APMAP expression was closely related to TNM stage, distant metastasis, and tumor differentiation. Functionally, APMAP knockdown repressed NSCLC cell proliferation and invasion, and induced cell ferroptosis. Mechanistically, transcription factor YY1 induced APMAP expression. Meanwhile, APMAP expressions were decreased after interfering with YY1, while APMAP expressions were increased after overexpressing YY1. Also, co-transfection experiments demonstrated that YY1 overexpression enhanced the fluorescence intensity of APMAP-WT promoter. Importantly, YY1 overexpression promoted NSCLC cell proliferation and invasion, and repressed cell ferroptosis, yet these effects were reversed after APMAP knockdown. Moreover, knocking down APMAP reduced NSCLC proliferation in vivo, mainly through reduced tumor volume, reduced KI-67 and GPX4 expressions, and decreased p-pI3K, p-AKT, and p-mTOR protein levels. APMAP regulated by YY1 transcription enhanced NSCLC proliferation, invasion, and repressed cell ferroptosis via activating PI3K/AKT/mTOR. - Source: PubMed
Publication date: 2026/01/07
Zhuang XiaohongLin ShuZhang Cheng-ShengQin QiYan QixingLuo Jing-RuTang Wenjun - Gastric cancer (GC) remains a global clinical challenge due to late diagnosis, high heterogeneity, and poor prognosis. Tumor stemness has emerged as a key factor driving tumor aggressiveness and therapeutic resistance. However, the systematic characterization of high-stemness GC cells and their molecular features remains limited. We integrated single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, and bulk RNA-seq data to identify and characterize high-stemness GC cells. Stemness scores were calculated using CytoTRACE, and malignant cells were classified into high stemness (top 25% CytoTRACE-scored cells, HighStem), dynamic transition stemness (DTStem), and low stemness (LowStem) subpopulations based on the quartile method cutoff. ScPagwas and cell-cell communication profiling were used to explore genomic instability, genetic susceptibility, and microenvironmental interactions. HighStem-specific co-expression modules were identified via high-dimensional WGCNA (hdWGCNA), and features were screened using six machine learning algorithms. A benchmark model was constructed for HighStem prediction and interpreted using SHAP analysis. HighStem GC cells exhibited enhanced intercellular signaling, metabolic reprogramming, and stemness-related pathway activity. Five genes-APMAP, MAPRE1, GLB1, TSPAN6, and CDKN2A-were identified as robust HighStem features. Spatial and bulk transcriptomic validation confirmed their tumor-specific expression and prognostic relevance. The Support Vector Machine (SVM) model incorporating these genes achieved high accuracy (AUC = 0.973) in distinguishing HighStem cells, demonstrating strong clinical utility at the scRNA-seq level. In addition, experimental validation through knockdown of core genes (APMAP, CDKN2A, TSPAN6, MAPRE1, and GLB1) in SGC7901 and HGC-27 gastric cancer cell lines revealed a significant reduction in JAK1-STAT3 pathway activity, supporting their functional involvement in tumor stemness regulation. Furthermore, knockdown of these genes increased the sensitivity of GC cells to chemotherapeutic agents like 5-FU and cisplatin, indicating their potential role in chemoresistance. This study provides a comprehensive molecular and functional characterization of high-stemness GC cells. The identified signature genes and predictive models offer novel insights into GC stemness biology and could guide personalized therapeutic strategies. Furthermore, our findings suggest that the core genes identified in this study may serve as potential biomarkers for predicting treatment outcomes and monitoring therapeutic resistance in GC. - Source: PubMed
Publication date: 2025/12/17
Wang ZiyiLi XuehaoWang JinYu HuidongZhao DefengXu YanZhou SiyuMen Wanfu - Ischemic stroke is associated with widespread and dynamic brain structural alterations, but the relationship between these changes and underlying molecular signatures across different post-stroke stages remains unclear. Therefore, we examined the brain structural difference of patients with 3 T high resolution magnetic resonance, further explored special molecular signatures across ischemic stroke recovery stages. - Source: PubMed
Publication date: 2025/11/19
Chen XiuenLiang JialanDeng ChengdiYu ZhilinYe ZimingQin ChaoTang Yanyan - Tumor cells experience endoplasmic reticulum (ER) stress due to oncogene activation and stressors in the tumor microenvironment, such as hypoxia and acidosis. ER stress plays a crucial role in carcinogenesis. However, its oncogenic mechanism in esophageal squamous cell carcinoma (ESCC) remains poorly understood. - Source: PubMed
Publication date: 2025/07/31
Su FangyuYang XiaYan ZhaoyangWu JunhongLi XiaoxuXu TongxinXu HuanchenWang XinhaoHu ZhaokunLu JuntaoGuo Wei