Human Interleukin 24,IL-24 ELISA KIT
- Known as:
- Human Interleukin 24,Interleukin-24 Enzyme-linked immunosorbent assay test KIT
- Catalog number:
- 201-12-2163
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Interleukin 24 IL-24 ELISA KIT
Related genes to: Human Interleukin 24,IL-24 ELISA KIT
- Gene:
- IL24 NIH gene
- Name:
- interleukin 24
- Previous symbol:
- ST16
- Synonyms:
- mda-7, IL10B, Mob-5, C49A, FISP, IL-24
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-02
- Date modifiied:
- 2016-10-05
Related products to: Human Interleukin 24,IL-24 ELISA KIT
Related articles to: Human Interleukin 24,IL-24 ELISA KIT
- Oxaliplatin-based chemotherapy is a principal treatment for colon cancer, but drug resistance hinders its efficacy. Cancer cell dormancy is reportedly a crucial driver of chemoresistance. IL-24 functions vitally in tumor chemoresistance, yet its role in colon cancer dormancy and oxaliplatin resistance remains unexplored.IL-24 expression was assessed in colon cancer tissues and cells via RT-qPCR, western blotting, or immunohistochemistry. The functions of IL-24 in colon cancer cell proliferation, apoptosis, dormancy, and oxaliplatin resistance were evaluated by CCK-8, flow cytometry, and western blotting. The downstream mechanism of IL-24 was predicted using RNA sequencing and bioinformatics analyses and verified in vitro. A tumor xenograft mouse model was built to further verify the role of IL-24 in colon cancer. IL-24 was overexpressed in oxaliplatin-resistant colon cancer tissues and cells. Furthermore, IL-24 treatment reversed the anti-proliferative and pro-apoptotic effects of oxaliplatin on colon cancer cells. Regarding cell dormancy, IL-24 treatment triggered G0/G1 cell cycle arrest and upregulated dormancy markers (CDKN1A, CDKN1B, TGFB2, and MSK1). Bioinformatics analyses revealed that IL-24 might function in colon cancer mainly through NF-κB pathway, and IL-24 activated the NF-κB axis in tumor cells. Importantly, treatment with NF-κB inhibitor reversed IL-24-induced colon cancer cell dormancy and oxaliplatin resistance. In vivo, IL-24 treatment abolished the anti-tumor effects of oxaliplatin, promoted cell dormancy, and activated NF-κB signaling in tumor tissues. IL-24 induces colon cancer cell dormancy and oxaliplatin resistance by activating NF-κB signaling. The IL-24/NF-κB axis may serve as a likely target to alleviate oxaliplatin resistance in colon cancer. - Source: PubMed
Publication date: 2026/07/16
Hu YanyanLi ShengyingZhu MinjingGong ChaojuFang Zejun - Crohn's disease (CD) is a chronic inflammatory condition of the gastrointestinal tract, where oxidative stress is a significant contributing factor to its pathogenesis. This study utilized multi-omics data, including RNA sequencing from the GSE216447 dataset and three genome-wide association studies (GWAS) datasets (ieu-a-10, ieu-a-11, ieu-a-13), to investigate the molecular networks related to oxidative stress in CD. Differential expression analysis was performed using DESeq2, followed by pathway enrichment analysis with clusterProfiler. Protein-protein interaction (PPI) networks were constructed using the STRING database. Mendelian Randomization (MR) analysis was conducted using TwoSampleMR and MRMix to identify causal relationships between genetic variants and CD. Quantitative real-time polymerase chain reaction (qPCR) was further applied to verify key differentially expressed genes (DEGs), including FASN, HMGCR, ASCC3, CD101, ELOVL6, PHLDA2, PHLDA3, and SCPEP1, in intestinal mucosal samples from both inactive and active CD patients. The analysis identified 64 up-regulated and 46 down-regulated differentially expressed genes (DEGs) in response to HO intervention. Key pathways related to oxidative stress, including the p53 signalling pathway and steroid biosynthesis, were significantly enriched. Consistent with transcriptomic data, qPCR confirmed that FASN and HMGCR were significantly upregulated in inactive CD, while ASCC3, CD101, ELOVL6, PHLDA2, PHLDA3, and SCPEP1 were markedly increased in active CD (all p < 0.05). The MR analysis revealed that in the dataset ieu-a-10, ABCB9 and OSGIN1 were identified as having a significant causal relationship with CD using TwoSampleMR, while only OSGIN1 was significant in MRMix. In dataset ieu-a-11, ARL4C, CD101, HMGCR, and IL24 were found to be significantly associated with CD, with overlapping findings between TwoSampleMR and MRMix. For dataset ieu-a-13, ACTA2 and CD101 were consistently identified as significant, suggesting their potential roles in CD pathogenesis. The findings highlight the crucial involvement of oxidative stress-related molecular networks in CD and underscore the utility of Mendelian Randomization in elucidating causal genetic factors. qPCR validation confirmed persistent upregulation of lipid metabolism genes in inactive CD and significant elevation of inflammation-related genes in active CD, reinforcing the link between oxidative stress and disease activity. - Source: PubMed
Yang JuanZhang LidaWang XiaqingYang Yuxiu - Chronic obstructive pulmonary disease (COPD) exacerbation is a common respiratory condition, particularly when accompanied by eosinophilia, which mediates inflammatory responses that significantly impair the integrity of the airway mucosal barrier. This study aims to elucidate the roles of interleukin-24 (IL-24) and eosinophils (EOS) in COPD-associated tissue remodeling, focusing on their effects on the expression of pro-inflammatory mediators and extracellular matrix (ECM) components in pulmonary fibroblasts, as well as the underlying molecular mechanisms. Based on the differential expression of IL-24 between healthy individuals and COPD patients and its correlation with EOS, we differentiated EOL-1 cells into EOS using butyrate and established a co-culture system with pulmonary fibroblasts. Concurrently, groups of fibroblasts were stimulated with varying concentrations of IL-24 alone. The regulatory effects on pro-inflammatory mediators and ECM expression were systematically analyzed using flow cytometry, real-time quantitative polymerase chain reaction, enzyme-linked immunosorbent assay, immunofluorescence, and Western blotting. Under the present experimental conditions, IL-24 treatment was associated with enhanced fibrotic responses in pulmonary fibroblasts. Furthermore, compared with butyrate treatment alone, the combination of IL-24 and butyrate further increased the differentiation rate of EOL-1 cells into EOS cells. Differentiated EOS further stimulated pulmonary fibroblasts to secrete pro-inflammatory factors IL-6 and IL-8, as well as the tissue remodeling-related factor vascular endothelial growth factor (VEGF), thereby exacerbating the fibrotic process. This study confirms that IL-24 promotes the maturation and differentiation of EOL-1 cells and can induce a fibrotic phenotypic transformation in pulmonary fibroblasts. This interaction participates in regulating inflammatory responses and tissue remodeling during COPD progression, highlighting the critical role of eosinophil-fibroblast crosstalk in the pathological mechanisms of the disease. - Source: PubMed
Publication date: 2026/07/15
Cao XuetingLi RuiLin ChenyuLi BingyuGuo ZongweiKong XiangruiJiang LinaXiao Li - Combined immune checkpoint inhibitor (ICI) and chemotherapy is the standard first-line treatment for advanced non-small cell lung cancer (NSCLC) without targetable driver mutations. However, reliable biomarkers predictive of clinical benefit are lacking. We analyzed 54 patients with advanced NSCLC treated first-line with ICI plus chemotherapy. Pretreatment tumor biopsies underwent targeted DNA and RNA-seq. Plasma samples for circulating tumor DNA (ctDNA) profiling were collected at multiple timepoints. Associations between genomic, transcriptomic, and ctDNA features and objective response rate (ORR) and progression-free survival (PFS) were assessed. Genomic analysis revealed that mutations predicted longer PFS (HR = 0.35, = 0.034), whereas mutations were associated with shorter PFS (HR = 5.39, = 0.001). Exploratory transcriptomic analysis identified high and expression as predictors of poor prognosis, while high expression correlated with longer PFS. CD8 effector memory T-cell infiltration was significantly higher in responders ( = 0.029). Longitudinal ctDNA analysis showed that positivity at C2D1 (HR = 5.18, = 0.004), C3D1 (HR = 17.81, < 0.001), and C4D1(HR = 3.91, = 0.018) was associated with inferior PFS. This multi-omics analysis highlights the potential of integrating genomic, transcriptomic, and ctDNA biomarkers to optimize immunotherapy strategies in NSCLC. - Source: PubMed
Publication date: 2026/07/06
Li LailingHan DandanZhang XiaoliangZhou HuiLi JiajunTian TianBai RubingXu KeXu YehongHe ChengXu LinjuanWang HaoTang HaoWei SongLi JunHe RuiNiu ShichengGao XiWang FufengJing QifanYin JianiXu LingXu LinglingZhang Zhi-Hong - (SA) colonization and cigarette smoking are both implicated in the pathogenesis of chronic airway disease, yet their combined effects on epithelial responses remain unclear. We investigated transcriptomic changes in human bronchial epithelial cells (BEAS-2B) following co-exposure to SA and cigarette smoke extract (CSE). RNA sequencing revealed that combined SA+CSE co-exposure was associated with a marked increase in differentially expressed genes, compared with single exposures. Functional enrichment and network analyses identified significant activation of pathways related to neutrophil migration, extracellular matrix remodeling, and inflammatory cascades, including TNF and IL-17 signaling. Key hub genes, notably CCL20, CXCL1, CXCL8, and IL-24, showed marked synergistic upregulation, which was validated by quantitative RT-PCR. These findings suggest that SA and cigarette smoke co-exposure is associated with a transcriptomic profile suggestive of neutrophilic inflammation. The involvement of IL-24 and IL-17 signaling suggests potential pathways linking bacterial colonization and smoking to airway inflammation and remodeling. - Source: PubMed
Publication date: 2026/05/13
Won Ha-KyeongLee JiwonYun Jae WonPark Kyung EunLee Ji-HyangCho You SookCho Sang HeonChung Kian FanBachert ClausChoi Jun-PyoSong Woo-Jung