Proteins CXCL12 19-93_SDF-1 β , Human
- Known as:
- Proteins CXCL12 19-93_SDF-1 β , Human
- Catalog number:
- C120
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins CXCL12 19-93_SDF-1 β Human
Related genes to: Proteins CXCL12 19-93_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 19-93_SDF-1 β , Human
Related articles to: Proteins CXCL12 19-93_SDF-1 β , Human
- Cancer-associated fibroblasts (CAFs) play important roles in breast cancer (BC) progression and metastasis. Here we investigated whether CAFs from indolent vs. aggressive BCs differ in gene expression profiles and how they impact metastasis. - Source: PubMed
Publication date: 2026/04/17
Miller Philip CSharma UtsavTao JiaXiangSun JunMedina-Saenz KelsiePicon-Ruiz ManuelMorata-Tarifa CynthiaBare Susan MSlingerland Joyce MEl-Ashry DorrayaLippman Marc E - Pancreatic ductal adenocarcinoma (PDAC) is among the most aggressive and metastatic malignancies worldwide. Migrating cancer stem cells (miCSCs), marked by CD133⁺CXCR4⁺ expression is a key driver of PDAC progression, which currently lack effective therapeutic targets. Activated pancreatic stellate cells (PSCs) within the tumor microenvironment secrete CXCL12, the ligand for CXCR4, thereby promoting stemness, epithelial-to-mesenchymal transition (EMT), and chemoresistance in miCSCs. Despite advances in understanding PDAC biology, clinically effective strategies that target CXCR4⁺ CSC populations remain limited. In order to investigate the molecular mechanisms sustaining miCSCs, we performed protein-protein interaction network analysis, which identified the transcription factor BMI1 as a key downstream effector of the CXCL12/CXCR4 axis. Functional studies using shRNA-mediated knockdown of CXCR4 and BMI1 were conducted to assess their roles in miCSC migration, EMT, and self-renewal. We further evaluated the therapeutic potential of the endogenous CXCR4 antagonist EPI-X4 and its optimized derivative JM#21 in PDAC cell lines. We addressed the peptide stability by encapsulating JM#21 into mesoporous silica nanoparticles (MSNs) designed for improved half-life and sustained release under physiological conditions. BMI1 was confirmed as a critical mediator of CXCL12/CXCR4-driven stemness and EMT. Knockdown of CXCR4 or BMI1 significantly impaired miCSC maintenance and migration towards CXCL12. Both EPI-X4 and JM#21 potently inhibited CXCL12-mediated signaling, reduced EMT and stemness markers, and suppressed miCSC migratory potential. JM#21 displayed superior efficacy and re-sensitized previously resistant PDAC cell lines to gemcitabine and paclitaxel. Functional assays demonstrated that nanoparticle-loaded JM#21 more effectively suppressed EMT markers and self-renewal than the free peptide, highlighting the advantage of nanoparticle delivery in therapeutic applications. Given their biocompatibility and modularity, silica nanoparticles offer a promising platform for stabilizing peptide drugs. Our findings reveal that tumor-stroma crosstalk via the CXCL12/CXCR4/BMI1 axis plays a central role in sustaining miCSC-driven metastasis and therapy resistance in PDAC. Targeting this signaling pathway with nanoparticle-stabilized JM#21 represents a novel and clinically promising therapeutic strategy to disrupt PDAC progression and improve the efficacy of existing combination treatments. - Source: PubMed
Publication date: 2026/04/16
Tiwary KanishkaLahusen AntonInaas SyedaBeitzinger BastianSchmid RomanHarms MirjaHauff StefanieArnold FrankWalter KarolinAlcala SoniaHahn StephanHeßmann ElisabethKleger AlexanderAzoitei NinelSeufferlein ThomasSainz BrunoMünch JanLindén MikaHermann Patrick C - Small cell lung cancer (SCLC) is a recalcitrant malignancy with limited responses to immunotherapy, largely due to its uniquely immunosuppressive tumor microenvironment (TME). However, the molecular mechanisms driving this phenotype remain incompletely understood. - Source: PubMed
Publication date: 2026/04/16
Zeng PengLi Hai-FengShu Wen-BinZhang JingZhao Tian-ChengHu Jun-WenWang Jun-FuWang ChengLu Qing-YunYang Jia-HuiAn Yan-LiChen Rong - Acute respiratory distress syndrome (ARDS) has a high clinical mortality rate and continues to draw research attention regarding its mechanisms and potential treatments. Disruption of the endothelial barrier is a primary pathological feature, and glycocalyx degradation is a key factor contributing to this disruption. Human umbilical cord mesenchymal stem cells (hucMSCs) exhibit strong anti-inflammatory and immunomodulatory effects, making their application in ARDS treatment an area of increasing interest. Proteomic screening identified Cxcl12 as a protein secreted by hucMSCs. In male C57 mice and cell models, lipopolysaccharide (LPS) was used to induce injury, followed by interventions with hucMSCs or hucMSCs with silenced Cxcl12 to assess glycocalyx-related proteins SDC-1, HS, and the repair marker EXT-1. To evaluate downstream signaling, the CXCR4 receptor was inhibited and related indicators were examined. Silencing Cxcl12 reduced the therapeutic effect of hucMSCs on LPS-induced glycocalyx damage. Inhibition of CXCR4 also weakened the effect of Cxcl12. These findings indicate that hucMSCs alleviate LPS-induced glycocalyx damage in pulmonary vascular endothelial cells by secreting Cxcl12, which activates the downstream receptor CXCR4, providing a therapeutic effect for ARDS. - Source: PubMed
Publication date: 2026/04/16
Cui JinfengPeng ZhenyiChen YuanyuanLiu WeiChen QiuwenWang XiaozhiWang TaoHuang XiaoSun Ting - Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by profound metabolic perturbations and dysregulated crosstalk between immune cells and fibroblast-like synoviocytes (FLS). Phenylalanine (PHE), an aromatic amino acid, has been implicated in RA-related metabolic disorders, but its direct immunomodulatory effects on human primary FLS and peripheral blood lymphocytes remain unclear. This study aimed to identify RA-specific metabolic signatures via untargeted metabolomics and validate PHE's functional role in regulating core pathogenic cells in RA. - Source: PubMed
Publication date: 2026/04/15
Shen JinquanGao XuPan WeiYeFang ZhengYuWang XiaoChengWang Qingwen