Proteins CXCL12 22-93_SDF-1 β , Human
- Known as:
- Proteins CXCL12 22-93_SDF-1 β , Human
- Catalog number:
- C122
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins CXCL12 22-93_SDF-1 β Human
Related genes to: Proteins CXCL12 22-93_SDF-1 β , Human
- Gene:
- CXCL12 NIH gene
- Name:
- C-X-C motif chemokine ligand 12
- Previous symbol:
- SDF1A, SDF1B, SDF1
- Synonyms:
- SCYB12, SDF-1a, SDF-1b, PBSF, TLSF-a, TLSF-b, TPAR1
- Chromosome:
- 10q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-30
- Date modifiied:
- 2016-10-05
Related products to: Proteins CXCL12 22-93_SDF-1 β , Human
Related articles to: Proteins CXCL12 22-93_SDF-1 β , Human
- Bone metastasis can remodel the bone marrow microenvironment, yet how metastatic tumors reshape hematopoiesis and immunity across marrow regions remains poorly defined. Here, we profile a cross-cancer single-cell atlas with 126,986 cells by integrating bone marrow samples (tumor, involved, and distal sites) from liver, prostate, and kidney cancer bone metastases, as well as benign controls, resolving 7 major lineages and 66 subpopulations. We identified coordinated immune suppression and niche remodeling that innate cells rose in peri-tumoral marrow but dropped in tumor sites, while adaptive T/B cells progressively depleted and stromal/epithelial compartments expanded. We further revealed a shift in myelopoiesis toward immunosuppressive monocyte/macrophage states with GMP-level lineage bias, alongside impaired erythropoiesis and B lymphopoiesis driven by myeloid-like reprogramming of precursors. Tumor sites were enriched with exhausted/stressed T cells, linked to inhibitory progenitor-T cell interactions (e.g., LGALS9-HAVCR2 and CLEC2-KLRB1). Non-hematopoietic support signals (CXCL12-CXCR4, ICAM1-SPN) were attenuated, and tumor programs included a marrow-specific metaprogram with IGFBP3/NAMPT signaling predicted to further destabilize the HSC niche. Overall, our study offers an integrated framework for decoding the metastatic marrow ecosystem by jointly targeting hematopoietic distortion, stromal collapse, and immune dysfunction. - Source: PubMed
Publication date: 2026/08/31
Shen ZhilongWang ShaoxuanJiang HaoWang PengruZhou ShangbinLi BoYuan HaoNi LiangweiMao YongxinXu GanLai BowenZhang HaoZhu ZhipengZhang XinXu ConglingXiao JianruXu Wei - Bone marrow Adipoq-lineage cells refer to all cells that have ever expressed Adipoq (Adiponectin) and their progeny. They contribute not only to marrow adipogenesis but also to osteoclast regulation, hematopoietic support, vascular maintenance, and post-injury regeneration. Recent single-cell transcriptomic and genetic fate-mapping studies have revealed unexpected heterogeneity within this lineage, such as genuine adipogenic precursors (MALPs), bipotent adipo-osteoprogenitors (AdipoqOsx cells), and their differentiated progeny (including mature marrow adipocytes and, in some contexts, osteoblasts). The progenitor subsets partly overlap with well-characterized SSPC subsets such as CXCL12-abundant reticular cells and leptin receptor-expressing cells, yet they exhibit distinct functional properties. This review synthesizes current knowledge on the identity, differentiation potential, and multifaceted functions of bone marrow Adipoq-lineage cells, with a focus on their roles in promoting osteoclastogenesis, regulating osteogenesis, supporting hematopoiesis and vascular integrity, and mediating bone marrow repair after injury. We also discuss how these cells are regulated by intrinsic factors that either control cell-autonomous fate or modulate secretory phenotype, and highlight key unresolved questions. By integrating these findings into a unified conceptual framework, this review aims to guide future research and therapeutic development targeting these cells in skeletal and hematopoietic disorders. - Source: PubMed
Publication date: 2026/08/13
Zhang ChunyanGu XiaohuiXiang YuyanZheng ChanchanYang LeiChen Jianquan - Metastatic breast cancer remains difficult to cure, and the way B and T lymphocytes adapt across metastatic niches especially under therapy remains insufficiently defined. Clarifying compartment specific immune remodeling may help explain resistance to PD-1/PD-L1 blockade and identify actionable targets. We performed an integrated meta-analysis of single cell RNA-seq datasets from normal breast tissue, primary tumors, tumor-draining lymph nodes (TLNs), and peripheral blood mononuclear cells (PBMCs), focusing on B and Tcell states. Immune composition differed notably by compartment. Tumors were enriched for effector CD8 states (CD8 cytotoxic 20.1%; CD8 activated 13.5%), whereas TLNs preserved larger naïve and memory reservoirs (CD4 naïve 40.7%; B naïve 11.4%; B memory 12.0%) and contained a higher B cell fraction than tumors (39.6% vs. 19.5%). Post therapy, PBMCs and TLNs showed increased BTLA-HVEM (TNFRSF14) checkpoint signaling and enhanced MIF-CD74 interactions with a shift from CD44 toward CXCR4, consistent with CXCR4 driven migratory and survival programs. In TLNs, TNFRSF14 signaling was unidirectional (B→T), absent in the reverse direction, and not detected in tumors. Clinically, higher tumor CXCR4 combined with lower TNFRSF14 was associated with shorter progression free survival in TCGA-BRCA, most evident in node positive, early stage disease. To target the BTLA-HVEM checkpoint axis, we performed structure guided peptide design using the native HVEM (23-39) peptide as an active structural template, followed by docking and molecular dynamics simulations. The optimized De novo-P2 peptide showed stable and favorable interactions at the BTLA interface, supporting its potential as a competitive modulator of BTLA-HVEM signaling. These data define niche specific lymphocyte remodeling and implicate BTLA-HVEM and CXCL12-CXCR4 as candidate biomarkers and therapeutic targets linked to PD-1/PD-L1 resistance. - Source: PubMed
Publication date: 2026/08/12
Khan SajidJamil SabahatHamza MuhammadAttique ZarlishZhang Suping - BACKGROUND Ischemic stroke causes severe neurological damage, and promoting angiogenesis in the ischemic penumbra is critical for neurovascular reconstruction and functional recovery. Astragaloside IV (AS-IV) and Tetramethylpyrazine (TMP) are a classic Chinese medicine combination for treating ischemic stroke, yet their synergistic mechanisms are unclear. This study aimed to investigate the enhanced effects of AS-IV combined with TMP on cerebral microvascular endothelial cells following ischemia-reperfusion injury and to explore the regulatory role of the lncRNA MALAT1-CXCL12/CXCR4 signaling axis. MATERIAL AND METHODS An oxygen-glucose deprivation/reperfusion (OGD/R) model was established using the bEnd.3 mouse brain microvascular endothelial cell line. Cells were treated with AS-IV, TMP, or their combination to evaluate therapeutic efficacy. Cell viability and migration capacity were assessed using CCK-8, wound healing, and Transwell assays. The expression levels of MALAT1 and angiogenesis-related markers (VEGFA, Ang1, Ang2, CXCL12, and CXCR4) were analyzed via qPCR, western blot, and immunofluorescence. To verify the mechanism, a stable MALAT1 knockdown model was constructed using lentiviral-mediated shRNA transduction. RESULTS OGD/R insult significantly reduced cell viability and migration, downregulated MALAT1 expression, and disrupted the Ang1/Ang2 balance. While AS-IV or TMP monotherapy partially mitigated these injuries, the combined treatment demonstrated a greater protective effect than either monotherapy. This enhancement was characterized by upregulation of MALAT1, activation of the CXCL12/CXCR4 pathway, and restoration of VEGFA and Ang1 protein expression. Furthermore, lentiviral-mediated MALAT1 silencing (shMALAT1) markedly impaired cell migration and angiogenic marker expression, effects that were partially rescued by the combined AS-IV and TMP intervention. CONCLUSIONS The combination of AS-IV and TMP exhibits an enhanced effect compared to either monotherapy in promoting endothelial migration and marker expression in vitro. These findings suggest that the protective mechanism is consistent with the involvement of the MALAT1-CXCL12/CXCR4 signaling axis. This study provides a preliminary cellular rationale for further in vivo validation of this combination therapy in rodent stroke models. - Source: PubMed
Publication date: 2026/08/27
Li GuangyaLu YunweiHuang LiulingZhu JingwenLi LilingLi PeizeLi ShanshanQin Xiude - : The efficacy of chemotherapy in triple-negative breast cancer (TNBC) is limited by intrinsic resistance and the tumor microenvironment (TME). Accumulating evidence reveals a mechanistic connection between programmed death-ligand 1 (PD-L1) and c-x-c motif chemokine receptor 4 (CXCR4), which dominate stroma barriers, immune escape, and cancer metastasis. Earlier studies have shown that dual suppression of c-x-c motif ligand 12 (CXCL12)/CXCR4 and programmed cell death-1 (PD-1)/PD-L1 pathways regulates extracellular matrix (ECM) deposition, activation of cancer-associated fibroblasts (CAFs), and epithelial-mesenchymal transition (EMT) of pancreatic cancer cells. : We combined BsNb PX4, a bispecific nanobody targeting PD-L1 and CXCR4, with paclitaxel or gemcitabine in multiple tumor cell lines and human peripheral blood mononuclear cell (hPBMC)-reconstituted xenograft mouse models. Antitumor activity was assessed by CCK-8, flow cytometry, and ELISA, and immune cell infiltration and TME remodeling were examined by immunofluorescence, immunohistochemistry, cytokine assays, and RNA-seq. : In MDA-MB-231 cells, BsNb PX4 synergistically enhanced paclitaxel-induced growth inhibition and apoptosis via G/M cycle arrest. This combinatorial strategy profoundly remodeled tumor immunity by expanding CD8 T cells and depleting Foxp3 CD4 regulatory T cells (Tregs), while concurrently restoring T-cell cytotoxicity and skewing the cytokine balance toward an antitumor state, with elevated IFN-γ and reduced TGF-β1. Notably, compared with paclitaxel monotherapy, the combination significantly elevated intratumoral CD8 T-cell infiltration, decreased Treg abundance, and exerted robust inhibitory effects on tumor growth and metastasis in humanized TNBC xenografts. : These findings reveal that dual blockade of PD-L1 and CXCR4 acts synergistically with chemotherapy by triggering tumor cell apoptotic effects and reversing the immunosuppressive microenvironment, thereby emerging as a promising therapeutic strategy for TNBC. - Source: PubMed
Publication date: 2026/08/14
Xu ShuyiHu HaiLi YifanZhang JiaweiWang LeiPaerhati PameilaBao WenxinBian YanlinZhu JianweiWu Mingyuan