CXCR4 Antibody
- Known as:
- CXCR4 Antibody
- Catalog number:
- 1009
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CXCR4 Antibody
Related genes to: CXCR4 Antibody
- Gene:
- CXCR4 NIH gene
- Name:
- C-X-C motif chemokine receptor 4
- Previous symbol:
- -
- Synonyms:
- LESTR, NPY3R, HM89, NPYY3R, D2S201E, fusin, HSY3RR, NPYR, CD184
- Chromosome:
- 2q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2019-04-23
Related products to: CXCR4 Antibody
Related articles to: CXCR4 Antibody
- Intrauterine adhesion (IUA) is a common complication of endometrial injury. Bone marrow mesenchymal stem cells (BMSCs) have been implicated in endometrial repair, but strategies to enhance their therapeutic efficacy remain to be optimized. The C-X-C chemokine receptor type 4 (CXCR4)/C-X-C motif chemokine ligand 12 (CXCL12) axis plays a pivotal role in BMSC homing. - Source: PubMed
Zhu LinhuaYue YongfangCao Lili - Peripheral blood mononuclear cell (PBMC) immunophenotyping has emerged as a promising non-invasive approach to characterize systemic immune alterations in cancer and to identify biomarkers associated with treatment response and resistance. However, current evidence remains fragmented and predominantly descriptive, with substantial heterogeneity in study design, immunophenotyping methodologies, and patient populations, limiting the identification of robust and clinically translatable immune signatures. In this review, we aim to comprehensively analyze PBMC immune phenotypes across multiple cancer types, with particular emphasis on their association with disease progression, therapeutic outcomes, and the key methodological and translational challenges that currently limit their clinical implementation. Across malignancies, conserved immune features are consistently observed, including T cell exhaustion, regulatory T cell (Treg) expansion, and upregulation of immune checkpoint molecules, reflecting chronic immune activation and dysfunction. In parallel, tumor-specific phenotype, such as peripheral helper T (Tph) cell expansion in non-small cell lung cancer, Vδ1CD69 γδ T cells in hepatocellular carcinoma, and T-cell immunoreceptor with Ig and ITIM domains (TIGIT) positive dysfunctional T cells in oral squamous cell carcinoma, highlight the influence of tumor-specific immune contexts. Importantly, this review moves beyond descriptive reporting by integrating mechanistic insights into how PBMC phenotypes contribute to therapeutic resistance. Key mechanisms include immunosuppressive cytokine signaling (e.g., interleukin-10 (IL-10), transforming growth factor-β (TGF-β)), chronic antigen stimulation driving T cell dysfunction, and systemic immune-tumor crosstalk mediated by chemokine axes such as stromal cell-derived factor 1 (SDF-1)/C-X-C motif chemokine receptor 4 (CXCR4). In addition to lymphoid populations, we emphasize the contribution of myeloid cell subsets, including monocytes and myeloid-derived suppressor cells, as central regulators of immune evasion and treatment failure. Despite these advances, significant challenges remain, including the lack of standardized protocols, limited longitudinal and multicenter validation studies, and insufficient integration of multi-omics approaches. Addressing these limitations will be essential for clinical translation. Overall, this review provides a refined conceptual framework that distinguishes conserved and tumor-specific immune signatures and highlights their mechanistic relevance in therapeutic resistance, supporting the development of PBMC immunophenotyping as a tool for personalized cancer immunotherapy. - Source: PubMed
Publication date: 2026/09/14
Olaechea AllinsonCamacho Rubio CristinaGómez-Melero Sara - Hepatocellular carcinoma (HCC) commonly develops in the context of chronic liver injury and fibrosis, and its immune evasion and therapeutic resistance are shaped not only by tumor-intrinsic factors but also by persistent interactions between the tumor stroma and immune cells. Hepatic stellate cells (HSCs) represent an important source of cancer-associated fibroblasts (CAFs) in HCC. HSC-derived CAFs can restrict the infiltration and function of effector T cells and promote the accumulation of immunosuppressive cells through CAF-associated and multicellular signaling networks, including TGF-β/SMAD, IL-6/STAT3, CXCL12/CXCR4, and CCL2/CCR2, as well as through extracellular matrix remodeling, vascular abnormalities, hypoxia, and metabolic reprogramming. Importantly, mediators such as IL-6 and CCL2 are not specific to HSC-derived CAFs and can also be produced by immune cells, hepatocytes, and other cellular populations within the HCC microenvironment. Conversely, cytokines released by distinct T-cell subsets, including IL-17A, TGF-β, IL-10, IFN-γ, and TNF-α, can in turn shape CAF activation, inflammatory states, and matrix-remodeling programs, thereby establishing a dynamic immune-stromal feedback loop. Focusing on the heterogeneity of CAFs and T cells, this review systematically summarizes the major mechanisms underlying bidirectional crosstalk between HSC-derived CAFs and T cells and their stage-specific roles in chronic liver injury, HCC initiation, progression, and therapeutic resistance. We further discuss potential therapeutic strategies involving CAF modulation, stromal remodeling, combination immunotherapy, and patient stratification. Current evidence suggests that this crosstalk axis may provide an important framework for understanding immune exclusion and therapeutic resistance in HCC. However, its clinical translation remains constrained by CAF heterogeneity, limited targeting specificity, insufficient causal evidence in humans, and safety concerns in the setting of underlying liver disease. - Source: PubMed
Publication date: 2026/09/07
Pan KechuanMa Chunlian - The clustering states of cell surface C-X-C chemokine receptor 4 (CXCR4) play a critical role in cancer metastasis. We previously reported a "Pro-Clustering Polymers (PCP)" system, P-BS-CM1 → P-CM2, for the treatment of metastatic triple-negative breast cancer (TNBC). Subsequent studies demonstrated that PCP enhanced CXCR4 blockade and metastasis suppression by disrupting CXCR4 association-disassociation dynamic equilibrium and shifting the receptor toward a hyper-clustered state. As an alternative strategy to disrupt this equilibrium, shifting CXCR4 toward a less clustered, more dispersed state, i.e., inhibiting CXCR4 clustering, remains largely underexplored. Herein, we developed a "De-Clustering Polymer (DCP)" system, P-BS-pHLIP, which introduces steric hindrance to block receptor-receptor interactions and thereby inhibits CXCR4 clustering. Side-by-side comparisons of DCP with our previously developed PCP system revealed that different modes of CXCR4 manipulation dictate divergent downstream biological outcomes. PCP preferentially impaired tumor cell motility by inducing mitochondrial dysfunction and energy depletion, whereas DCP preferentially reduced tumor cell adhesiveness by downregulating multiple adhesion molecules. Both PCP and DCP exert potent anti-metastatic efficacy in multiple TNBC metastatic models. Collectively, this study demonstrates that engineered polymeric systems that biophysically manipulate receptor clustering states, via either pro-clustering or de-clustering, represent promising therapeutic strategies for suppressing cancer metastasis. - Source: PubMed
Publication date: 2026/09/20
Liu ChendongShi JunzhuShi LikaiJia QingruiLiu JiaqiYan YueZhou MingluZhou ZhouHuang YuanLi Lian - Migration of lung cancer cells to distant sites is largely mediated by the CXCR4/CXCL12 axis. Meanwhile, 1,2,4-triazole derivatives have shown antiproliferative activity in lung cancer and have been reported to inhibit metastasis in pancreatic and breast cancer. - Source: PubMed
Publication date: 2026/08/18
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