Human CCL11 cDNA Clone
- Known as:
- Human CCL11 complementary Desoxyribonucleic acid Clone
- Catalog number:
- DC11782
- Product Quantity:
- 10 ug
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- Human CCL11 cDNA Clone
Related genes to: Human CCL11 cDNA Clone
- Gene:
- CCL11 NIH gene
- Name:
- C-C motif chemokine ligand 11
- Previous symbol:
- SCYA11
- Synonyms:
- eotaxin, MGC22554
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-24
- Date modifiied:
- 2016-10-05
Related products to: Human CCL11 cDNA Clone
Related articles to: Human CCL11 cDNA Clone
- Allergic rhinitis (AR) and asthma (AS) are closely linked in both epidemiology and pathogenesis, though the mechanisms remain unclear. This study aims to identify shared gene signatures and molecular mechanisms in the combined allergic rhinitis and asthma syndrome (CARAS) and validate these findings in a murine model. - Source: PubMed
Publication date: 2026/05/15
Wang ZhuiyueChen JingZhang YuanyuanZhao XiaomanShen ShipingZhang XinguangYao WenboLiu YazunXue Zheng - Lymph node metastasis (LNM) is a primary critical factor for gastric cancer (GC) prognosis, fundamentally driven by the adaptive remodeling of the tumor microenvironment (TME). While gastric cancer-associated mesenchymal stem cells (GCMSCs) are recognized as pivotal orchestrators of the tumor niche, the paracrine mediators governing LNM remain poorly defined. In this study, integrative transcriptomic and cytokine profiling identified CCL11 as the most significantly upregulated chemokine in GCMSCs. Clinical analysis demonstrated that elevated CCL11 expression in tumor tissues correlated with advanced LNM and dismal overall survival. Furthermore, a signature score derived from CCL11 MSC subclusters, identified via single-cell RNA sequencing, was positively associated with advanced clinical stages and poor prognosis. Serum CCL11 levels further exhibited high diagnostic efficacy for gastric cancer (AUC:0.8131) and moderate predictive value for lymph node metastasis (AUC:0.7848). Intriguingly, despite these robust clinical associations, exogenous CCL11 failed to directly influence the proliferative or migratory capacity of GC cell lines. This discrepancy was resolved by our finding that the cognate receptor CCR3 was virtually absent on the malignant epithelium but selectively enriched on macrophages and lymphatic endothelial cells (LECs). Functionally, GCMSC-derived CCL11 drove M2 macrophage polarization to bolster tumor stemness and chemoresistance, while simultaneously remodeling LECs to facilitate lymphangiogenesis and transendothelial migration. Mechanistically, hypoxic stress triggered the nuclear translocation of TCF21, which directly transactivated the CCL11 promoter in GCMSCs. Together, these findings identify the hypoxia-TCF21-CCL11 axis as a key driver of the GC metastatic niche, highlighting the indispensable significance of stromal-derived molecules in deciphering metastatic complexity and identifying promising targets for early diagnosis and strategic therapeutic intervention. - Source: PubMed
Publication date: 2026/05/13
Zhao XinlanHe ZhujingCao XiaoliLiu JiahuiDai ChunWang Mei - Eosinophils, traditionally viewed as effector cells in allergic and parasitic responses, have emerged as multifaceted regulators within the tumor microenvironment (TME). In lung cancer, eosinophils demonstrate complex and context-dependent functions, shaped by chemokines, cytokines, and tumor-derived signals such as CCL11 and IL-33. Recent studies indicate that eosinophils may either promote anti-tumor immunity, by enhancing CD8 T cell infiltration, secreting cytotoxic granules, and cooperating with IL-33, or facilitate tumor progression through recruitment of regulatory T cells, immune suppression, and expression of immunoregulatory enzymes like IDO. Moreover, eosinophil abundance in tumor tissues and peripheral blood has been associated with both favorable and unfavorable prognostic outcomes in lung cancer patients. Notably, elevated eosinophil counts correlate with improved responses to immune checkpoint inhibitors (ICIs), positioning them as potential biomarkers for immunotherapy efficacy. However, distinctions between tumor-infiltrating and circulating eosinophils, as well as their dualistic roles in metastasis and immune modulation, remain incompletely understood. This review summarizes current advances in understanding eosinophil biology in lung cancer and underscores their promise as diagnostic and therapeutic targets in precision immuno-oncology. - Source: PubMed
Publication date: 2026/04/28
Wang ZhenJiao FuzhiYuan JingZhang ShengnanShi Fenglei - : Recurrence poses a major challenge in epithelial ovarian cancer (EOC), often occurring despite optimal first-line therapy. Dormant cancer cells are believed to play a key role, yet the mechanisms driving their reactivation remain unclear. This study examined whether exosomes released by normal peritoneal mesothelial cells (PMCs) and fibroblasts (PFBs) undergoing iatrogenic senescence after carboplatin and paclitaxel exposure contribute to EOC recurrence. : Senescent PMCs and PFBs secreted markedly more exosomes, identified by CD9, CD63, and CD81, compared with young cells. Exosomes from both cell types more effectively reactivated dormant EOC cells (pEOCs, A2780, OVCAR-3, SKOV-3) than non-exosomal medium constituents. Importantly, senescent PMC-derived exosomes most strongly reactivated pEOCs and SKOV-3, whereas those from senescent PFBs exerted greater effects on pEOCs, OVCAR-3, and SKOV-3. Kinetic studies of exosome internalization revealed that this process was generally more efficient in the presence of exosomes derived from senescent cells compared with those from young donor cells. Compositional analysis revealed distinct profiles between young and senescent exosomes compared in two variants: young PMCs/senescent PMCs and young PFBs/senescent PFBS. Senescent PMC exosomes displayed reduced miR-210-3p, miR-409-3p, and miR-421, alongside elevated MMP1, MMP3, and VEGF, while senescent PFB exosomes showed increased amphiregulin and osteopontin but lower MMP1, MMP3, TIMP1, bFGF, VEGF, and HGF. Functionally, senescent PMC exosomes enhanced pEOC migration, invasion, and spheroid formation, and induced the expression of CCL11 and ABCB1. Senescent PFB exosomes promoted migration and upregulated CCL11, TGF-β1, BIRC5, and CHEK1. : These findings suggest that therapy-induced senescence in peritoneal cells may contribute to EOC recurrence by reactivating dormant tumor cells through exosomal signaling. - Source: PubMed
Publication date: 2026/04/23
Rutecki SzymonKrawiec AdriannaLeśniewska-Bocianowska AgnieszkaMatuszewska JuliaNaumowicz ErykSzubert SebastianKsiążek KrzysztofMikuła-Pietrasik Justyna - Allergic conjunctivitis (AC) is a prevalent ocular surface inflammatory disorder with limited therapeutic options. In this study, we investigated the role of colony-stimulating factor 1 receptor (CSF1R) in an ovalbumin (OVA)-induced murine model of AC. Conjunctival expression of CSF1R and its ligands, interleukin-34 (IL-34) and colony-stimulating factor 1 (CSF1), was significantly upregulated following OVA challenge. Pharmacological inhibition of CSF1R with BLZ945 alleviated clinical symptoms, reduced the infiltration of CD45⁺ leukocytes and eosinophils, and attenuated an M2-associated macrophage phenotype in the conjunctiva. Similar suppression of eosinophil infiltration was observed with a second CSF1R inhibitor, AZD7507. In addition, conjunctival CD206⁺ macrophages with an M2-associated phenotype expressed C-C motif chemokine ligand 11 (CCL11), which was elevated in AC and downregulated by CSF1R inhibition. Recombinant CCL11 significantly restored eosinophil infiltration in BLZ945-treated mice, supporting a role for CCL11 as a downstream effector of CSF1R signaling in this model. Collectively, these findings support a contributory role for CSF1R signaling in macrophage-associated eosinophilic inflammation in murine AC and suggest that targeting CSF1R may represent a potential therapeutic strategy for ocular allergic disease. - Source: PubMed
Publication date: 2026/05/08
Du JinghengWu JiaxinTan XiukuiXie JingbinZhuang ZhudanLan HuifeiXue YunxiaFu TingGu JingyiLi ZhijieLiu Jun