mAb mouse anti-human MCP-1
- Known as:
- mAb mouse (anti-) to-H. sapiens MCP-1
- Catalog number:
- CT691
- Product Quantity:
- 0.5 mg
- Category:
- -
- Supplier:
- U-CyTech
- Gene target:
- mAb mouse anti-human MCP-1
Related genes to: mAb mouse anti-human MCP-1
- Gene:
- CCL2 NIH gene
- Name:
- C-C motif chemokine ligand 2
- Previous symbol:
- SCYA2
- Synonyms:
- MCP1, MCP-1, MCAF, SMC-CF, GDCF-2, HC11, MGC9434
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-05
- Date modifiied:
- 2016-10-05
- Gene:
- SLC25A14 NIH gene
- Name:
- solute carrier family 25 member 14
- Previous symbol:
- -
- Synonyms:
- BMCP1, UCP5
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-09
- Date modifiied:
- 2016-10-05
Related products to: mAb mouse anti-human MCP-1
Related articles to: mAb mouse anti-human MCP-1
- Lung squamous cell carcinoma (LUSC) frequently metastasizes to lymph nodes, yet how tumor-intrinsic biomechanical cues influence nodal immune environments remains unclear. Here, we identify solid stress, generated during tumor expansion, as a key driver of pre-metastatic niche formation in tumor-draining lymph nodes (TDLNs). Using murine models with defined solid stress levels, we show that high-stress tumors induce early TDLN remodeling characterized by fibroblast activation and accumulation of immunosuppressive S100a8⁺ myeloid cells. Single-cell and spatial transcriptomics reveal that Col1a1⁺ fibroblasts upregulate STAT3 and YAP-dependent chemokines (CCL2, CSF1), establishing a fibroblast-myeloid signaling axis that supports myeloid recruitment and suppresses CD8⁺ T cell infiltration. Functional blockade of CCR2, CSF1R, STAT3, or YAP disrupts fibroblast-myeloid co-localization, restores antigen-presenting cell populations, and enhances CD8⁺ cytotoxic T cells activity, leading to reduced lymph node metastasis and improved survival. Mechanistically, chromatin accessibility and ChIP assays reveal direct binding of p-STAT3 and YAP at inflammatory enhancer elements in fibroblasts under mechanical strain. Cross-species spatial transcriptomic analysis confirms the inverse association between Col1a1⁺ fibroblast density and CD8A⁺ T cell presence in human LUSC tissues. Our findings uncover a mechano-immune circuit whereby tumor-derived solid stress activates fibroblast-STAT3/YAP signaling to remodel TDLNs into immunosuppressive, metastasis-permissive niches. Targeting this biomechanical axis offers a promising strategy to intercept early lymphatic dissemination in LUSC. - Source: PubMed
Publication date: 2026/06/17
Cai JieAn ZhaoGao WeiLi RyanChen Zhe-ShengLi AnZhu LeiShen Yingran - : Bladder cancer (BCa) is characterized by frequent recurrence and limited durable responses to immunotherapy, in part due to poor T-cell infiltration into tumors. While the chemokine CCL2 and its receptor CCR2 have traditionally been associated with recruitment of immunosuppressive myeloid cells and tumor promotion, we reveal an unexpected anti-tumor role for this pathway in BCa. : Using orthotopic and carcinogen-induced murine BCa models, we demonstrate that genetic deletion or antibody blockade of CCL2 or CCR2 accelerates tumor progression, reduces intratumoral CD4 and CD8 T-cell infiltration, and shortens survival. : Mechanistic studies show that CCL2 promotes recruitment of CCR2 effector T cells with enhanced activation and cytotoxicity. Mixed bone marrow chimeras, T-cell-specific CCR2 knockouts, and adoptive transfers confirm that CCR2 signaling within T cells is essential for their trafficking and anti-tumor function. In human BCa, CCL2 expression is reduced in tumors compared to adjacent urothelium, correlating with diminished T-cell infiltration. Importantly, high tumor CCL2 levels are associated with improved recurrence-free survival in patients with BCa. To therapeutically leverage this pathway, we developed a novel intravesical recombinant CCL2 (rCCL2) approach. rCCL2 delivery significantly increased CCR2 T-cell infiltration, reduced tumor burden, and extended survival in both syngeneic MB49 and double-humanized patient-derived xenograft (PDX) BCa models. : These findings redefine the CCL2-CCR2 axis as a T-cell-mediated tumor-suppressive pathway in BCa and support rCCL2-based therapy as a strategy to enhance immune infiltration and improve outcomes in treatment-resistant BCa. - Source: PubMed
Publication date: 2026/07/15
Mukherjee NeelamJi NiannianHassouneh ZainebFurman JaimeFisher OliviaGelfond JonathanNoel Onika D VMorales GiseleTan XiChen Chun-LiangWoldu Solomon LLotan YairSvatek Robert S - Ovarian cancer, particularly high-grade serous ovarian cancer (HGSOC), remains one of the most lethal gynecological malignancies due to late diagnosis and the development of chemoresistance. The tumor microenvironment (TME) plays an important role in disease progression, with chemokines influencing cell recruitment, angiogenesis, metastasis, and immune modification. This review synthesizes current evidence on key chemokine axes in ovarian cancer, highlighting their dual roles as prognostic biomarkers and therapeutic targets. The most important axes include CXCL12/CXCR4 (which drives tumor proliferation, angiogenesis and chemoresistance via epithelial-mesenchymal transition), CCL2/CCR2 (promoting immunosuppressive tumor-associated macrophages and resistance), and CCL5/CCR5 (enhancing pro-oncogenic signaling and Treg/MDSC infiltration). Pro-angiogenic ELR+CXC chemokines like CXCL8 induce vascularization and inflammation. On the contrary, effector chemokines (CXCL9/10/11/13) correlate with "hot" immune subtypes and improved survival in several studies. High expression of immunosuppressive chemokines predicts poorer prognosis and therapy resistance, while immune-attracting profiles associate with better outcomes and chemotherapy responsiveness. Therapeutically, inhibitors like plerixafor (CXCR4), PF-04136309 (CCR2), and maraviroc (CCR5) show preclinical promise, synergizing with chemotherapy, anti-VEGF, and checkpoint inhibitors. Chemokines also represent actionable molecular targets to overcome ovarian cancer's "cold" immune phenotype. Future research should validate multi-chemokine signatures for patient stratification and advanced clinical trials toward personalized therapies. - Source: PubMed
Publication date: 2026/06/30
Długaszek AnnaKabut JacekDomagała-Haduch MałgorzataGorzelak-Magiera AnitaSadurska JoannaMorawiec Maria-LauraMielczarek-Palacz AleksandraGisterek-Grocholska Iwona - Acute liver injury (ALI) can rapidly progress to life-threatening acute liver failure. Liver transplantation remains the only definitive treatment, despite critical donor shortages. Macrophage-based therapies have shown promise in ALI but face challenges related to subset imprecision and limited humanized validation. VSIG4 is generally considered a marker of Kupffer cells; however, it is also expressed in monocyte-derived macrophages (MoMFs), and its role remains unclear during ALI. - Source: PubMed
Publication date: 2026/07/20
Duan BiaoChen JunLiu GuanLin JiachengYang ShiyuKong XiaoniRong WeifangTan Weifeng - Obesity significantly alters the adipose-tumor microenvironment and enhances colorectal cancer (CRC) progression. Visceral adipose tissue (VAT) becomes metabolically and immunologically activated, driving adipocyte dedifferentiation into cancer-associated adipocytes (CAAs). CAAs secrete adipokines, cytokines, chemokines, and lipid substrates that activate the JAK/STAT3, NF-κB, PI3K/AKT, and HIF-1α pathways in CRC cells, thereby enhancing proliferation, the epithelial-mesenchymal transition (EMT), angiogenesis, and immune escape. Increased fatty acid release and CD36/FABP-mediated uptake further support metabolic rewiring and metastatic potential. Key chemokine axes, CCL2/CCR2, CCL5/CCR5, and CXCL12/CXCR4, coordinate stromal recruitment and organ-specific dissemination, linking VAT inflammation to metastasis. New therapeutic concepts - including inhibition of lipid exchange between adipocytes and tumor, modulation of adipokine and chemokine signaling, and reprogramming of the CAA phenotype - highlight the clinical potential of targeting adipose-mediated tumor progression. In this review, we summarize and systematize the current mechanistic evidence on the interactions between adipose tissue and CRC, highlighting their importance in metastasis and therapy resistance. Despite significant progress, key aspects of adipose tissue modulation of CRC biology remain unexplored, underscoring the need for further mechanistic and translational research. - Source: PubMed
Publication date: 2026/07/17
Litwiniuk AnnaKalisz MałgorzataStępień DominikaSławkowska NataliaRoszkowski RafałRemyzovska OlgaGrala BartłomiejBik WojciechKwiatkowski Andrzej