Ask about this productRelated genes to: CD44 antibody
- Gene:
- CD44 NIH gene
- Name:
- CD44 molecule (Indian blood group)
- Previous symbol:
- MIC4, MDU2, MDU3
- Synonyms:
- IN, MC56, Pgp1, CD44R, HCELL, CSPG8
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
Related products to: CD44 antibody
Related articles to: CD44 antibody
- Although intracellular delivery via endocytosis is a promising strategy for drugs acting in the cytosol or nucleus, many macromolecular therapeutics remain trapped within endosomal/lysosomal compartments, limiting efficient cytosolic delivery. In this study, we designed a novel functional hyaluronic acid (HA)-based polymer, HA-octahistidine (His8), by conjugating His8 to CD44-targeting HA, and evaluated its physicochemical properties, cellular uptake, and endosomal escape capability. HA-His8 was synthesized via 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide/N-hydroxysuccinimide (EDC/NHS)-mediated coupling and characterized using H NMR spectroscopy. Particle size and zeta potential were measured via dynamic light scattering, and buffering capacity was evaluated using acid-base titration. Cellular uptake and intracellular localization were investigated in CD44-high MDA-MB-231 and CD44-low MCF-7 cells via confocal laser scanning microscopy. Cytotoxicity was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Successful conjugation of His8 was confirmed with a degree of substitution of 4.66 mol% relative to HA carboxyl groups. HA-His8 exhibited a nanoscale hydrodynamic diameter under physiological conditions, which increased under acidic conditions together with changes in zeta potential. HA-His8 exhibited higher buffering capacity than free His8 and was preferentially internalized by CD44-high MDA-MB-231 cells compared with MCF-7 cells. Compared with unmodified HA, HA-His8 exhibited lower colocalization with LysoTracker that decreased over time, indicating reduced retention within acidic vesicles. HA-His8 also exhibited low cytotoxicity over the tested concentration range. His8 modification alters HA intracellular localization while preserving CD44 targeting, thereby facilitating endosomal escape. These findings highlight HA-His8 as a potential platform for the cytosolic delivery of macromolecular therapeutics, including proteins, peptides, and nucleic acids. - Source: PubMed
Publication date: 2026/09/10
Yukimura TomonaIto HironoSuzuki TakahiroSeki ToshinobuSeki Tomohiro - Zeb1 is a well-known epithelial-mesenchymal transition (EMT) transcription factor and is highly expressed in aggressive cancers. Tumor hybrids, which were derived from fusion events between cancer cells and normal cells, such as macrophage and stem cells, can possess novel properties, such as enhanced metastatic activity. The role of Zeb1 was studied in M13-MDA231-6 and -13 tumor hybrids that were derived from spontaneous fusion events between MDA-MB-231-Hyg human breast cancer cells and M13SV1-EGFP-Neo human breast epithelial cells. The stable CRISPR/Cas9-mediated Zeb1-KO was correlated with re-expression of E-Cadherin in MDA-MB-231-Hyg-Zeb1-KO and M13-MDA231-13-Zeb1-KO cells, but not in M13-MDA231-6-Zeb1-KO cells. Similarly, the proliferation of MDA-MB-231-Hyg-Zeb1-KO in M13-MDA231-13-Zeb1-KO cells, but not in M13-MDA231-6-Zeb1-KO cells, was decreased as compared to non-edited cells. The migratory activity of Zeb1-KO cells was markedly reduced in transmigration and invasion studies compared to non-edited cells. However, MDA-MB-231-Hyg-Zeb1-KO cells and M13-MDA231-6-Zeb1-KO tumors only showed reduced migratory behavior in a scratch/wound healing assay, while M13-MDA231-13-Zeb1-KO exhibited enhanced locomotory activity. In contrast, no clear effects of Zeb1 knockout were observed on colony-forming capacity or CD44+/CD104+ expression. In summary, our data support the role of Zeb1 as a driver of EMT and cancer cell migration. - Source: PubMed
Publication date: 2026/09/16
Wörner Ida FriederikeDittmar Thomas - Breast cancer stem cells (BCSCs) drive tumor progression, metastasis, and therapeutic resistance. Sirtuin 1 (SIRT1) has been implicated in stem cell regulation, but its context-dependent role in BCSC maintenance and the underlying molecular mechanisms remain poorly defined. SIRT1 expression was evaluated in human breast cancer specimens. Pharmacologic and genetic SIRT1 inhibition was assessed in breast cancer cell lines and orthotopic xenograft models to determine effects on stemness, epithelial-mesenchymal transition (EMT), metastasis, and chemoresistance, with emphasis on Wnt/β catenin signaling. SIRT1 was overexpressed in breast cancer and correlated with higher tumor grades. SIRT1 inhibition reduced BCSC markers (CD44, ALDH1), stemness genes (NANOG, SOX-2), mammosphere formation, EMT, and invasion. In vivo, SIRT1 inhibition suppressed tumor growth, blocked lymphatic metastasis, and delayed cisplatin resistance. Mechanistically, these effects were mediated by downregulation of Disheveled 3 (DVL3) and attenuation of Wnt/β catenin signaling. SIRT1 is associated with the maintenance of BCSC-related properties, EMT, and activation of the Wnt/β-catenin pathway in breast cancer. Targeting SIRT1 may represent a potential therapeutic strategy to suppress tumor progression and improve treatment response. - Source: PubMed
Publication date: 2026/09/15
Ding JianminGuan BaoxiangFan XuejunZhang NingyanSevick EvaZhang Songlin - Lung cancer recurrence and therapeutic resistance are driven by cancer stem cells (CSCs), yet clinically available CSC-targeted therapies remain lacking. To identify actionable anti-CSC agents, we screened 1018 FDA-approved drugs using a 3D sphere culture system enriching lung CSC-like cells. Trimebutine, a gastrointestinal motility regulator targeting G-protein-coupled receptors (GPCRs), was identified as a potent agent with over 49.5-fold higher selectivity toward lung CSC-like cells (SI > 49.55) compared with standard therapies such as cisplatin (SI = 1.39) and gefitinib (SI = 1.00). In H460-SP spheres, trimebutine markedly impaired sphere-forming capacity, reduced cell viability, and downregulated key CSC surface markers (CD133, CD44) alongside stemness regulators (c-MYC, EpCAM, BMI1, OCT3/4, NANOG, SOX2, SMAD3). Mechanistically, trimebutine suppressed overexpressed calcium and potassium channels (, , , , ), attenuating downstream YAP/TAZ-TEAD signaling within the Hippo pathway to trigger apoptosis. In combination with cisplatin, trimebutine exhibited strong synergistic efficacy (Chou-Talalay combination index, CI = 0.015-0.228) in H460-SP spheres and patient-derived lung tumor organoids, suppressing cell viability, stemness marker suppression, and apoptotic cleavage of caspase-3 and PARP compared to monotherapies. Overall, trimebutine targets lung CSC populations by disrupting GPCR-ion channel-Hippo signaling crosstalk, providing a strong preclinical rationale for trimebutine-cisplatin combination strategies to overcome drug resistance and recurrence in lung cancer. - Source: PubMed
Publication date: 2026/09/15
Seo JiHyeLee HeejinChoi Dong KyuKim Young-KyuWoo SominLee ChangkyuChoi Jeong InJiang GeOh Bae JunLee Dong-SeokMin Sang-Hyun - Efficient cutaneous wound healing relies on the phenotypic transition of macrophages toward an anti-inflammatory, pro-reparative M2-like state. Non-healing chronic wounds are pathologically characterized by the breakdown of this polarization balance. In this review, we synthesize recent research on biomaterials fabricated from naturally occurring polysaccharides with intrinsic immunomodulatory activity, mainly represented by hydrogels that modulate macrophage phenotypic transitions. We first dissect the immune microenvironment of wound healing and elaborate on the core regulatory networks governing M1/M2 polarization, with a particular focus on signaling pathways and metabolic reprogramming. On this basis, we classify pro-M2 natural polysaccharides into mannose-containing and mannose-free categories according to their core structural motifs that mediate immunomodulatory activity, and detail their molecular mechanisms, including pattern recognition receptor engagement (MR, Dectin-1, CD44, etc.) and downstream signaling cascades (STAT6, PI3K/Akt, NF-κB, etc.). Representative polysaccharides such as konjac glucomannan (KGM), polysaccharide (GLP), chitosan (CS) and hyaluronic acid (HA) are discussed with a clarified structure-activity relationship (SAR). Finally, we highlight emerging design strategies for multi-functional immunomodulatory hydrogels, including mechano-biochemical coupling platforms and spatiotemporally controlled delivery systems, and analyze ongoing controversies and translational bottlenecks in this field. The relationship between material structure and function enables the rational design of purpose-built polysaccharide dressings that regulate immunity. This review highlights these materials as promising preclinical platforms for chronic wound management, although their clinical translation requires further validation. - Source: PubMed
Publication date: 2026/09/01
Huang ZheDi YuboWen LuyaoHe XingZhang WeiweiWei Qingcong