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
- Pancreatic tumors are characterized by a prominent desmoplastic stroma that can account for up to 90% of the tumor. Given the marked upregulation of CD44, a family of transmembrane glycoproteins, in pancreatic cancer-associated fibroblasts (CAFs), we investigated its role in regulating myofibroblastic and inflammatory CAF phenotypes. Conditional deletion of Cd44 in fibroblastic cells in Cd44;PdgfrβCreER mice significantly reduced tumor growth and was associated with a significant reduction in intratumoral regulatory T cells (T). Consistently, in human CAFs CRISPR/Cas9-edited to delete CD44, the fibroblasts' morphology changed drastically: CAFs lost their elongated phenotype and adopted a round shape, reflecting their inactivation. This was accompanied by a significant downregulation of activation markers, unresponsiveness to exogenous stimuli, and reduced contractile activity. Furthermore, CD44 ablation decreased extracellular matrix production and altered the immunomodulatory cytokine secretion, highlighting its role in both fibrosis and immune regulation. Finally, CD44-deficient CAFs exhibited a reduced capacity to suppress anti-tumor immune responses by failing to induce immunosuppressive programs in dendritic cells (DCs) and by increasing cytotoxic T cell (CTL)-mediated tumor cell killing. Collectively, we identify CD44 as a regulator of CAF activation and immunosuppressive function, linking stromal remodeling to immune evasion in pancreatic cancer and supporting CD44 as a potential therapeutic strategy to reprogram the tumor stroma and enhance anti-tumor immunity. - Source: PubMed
Publication date: 2026/08/15
Treffert Sven MátéHeneka Yvonne MadeleineMartin JulieGargano AlessandraLaunhardt LarissaAkilli ÖzlemStanganello ElianaAndrieux GeoffroyHoch DominiqueSonnentag Steffen JoachimMehner Lisa-MarieMunoz-Sagredo LeonelChrist MichelleOrian-Rousseau Véronique - Conventional oral nanocarriers for intestinal diseases rely on single-responsive mechanisms and target a single pathological stage, failing to address the inflammation-carcinoma continuum. Celastrol (Cel)'s oral translation is limited by poor bioavailability and lack of lesion-specific targeting. To overcome these barriers, we constructed a hyaluronic acid (HA)-functionalized platform featuring dual enzyme/ROS-triggered release and CD44-mediated active targeting (HA@Cel/NPs) for treating ulcerative colitis (UC), colitis-associated colorectal cancer (CAC), and colon cancer. - Source: PubMed
Publication date: 2026/08/10
Shi JinfengZhang XueqianYang LinxingWang WeiLiu LinglingLu TianXu XingXu YanRen ShiyuLuo Ruifeng - The high rates of recurrence and metastasis in colorectal cancer (CRC), coupled with its immunosuppressive tumor microenvironment (TME), severely constrain patient survival. To overcome the limitations of monotherapies, this study developed a multifunctional targeted nanoplatform (RLHMnH). This system consists of a hyaluronic acid (HA)-modified hollow manganese dioxide (H-MnO) nanocarrier co-loaded with the anti-angiogenic drug Regorafenib (Reg) and the nitric oxide precursor L-Arginine (L-Arg) for synergistic triple therapy against CRC. The platform leverages HA-mediated CD44 receptor targeting to achieve enhanced tumor accumulation. Within the TME, the H-MnO framework undergoes rapid responsive decomposition. On one hand, Within the acidic and GSH-rich TME, H-MnO undergoes reductive degradation to release Mn, concomitantly depleting GSH and disrupting redox homeostasis. The released Mn further catalyzes Fenton-like conversion of endogenous HO into highly cytotoxic ·OH, thereby inducing oxidative damage and tumor cell apoptosis. On the other hand, the concomitantly released Reg effectively blocks tumor angiogenesis by inhibiting the VEGFR2 signaling pathway, while L-Arg generates nitric oxide, synergistically reversing drug resistance, alleviating hypoxia, and activating anti-tumor immunity. Both in vitro and in vivo experiments demonstrated that RLHMnH, through integrating the triple synergistic mechanisms of CDT, anti-angiogenesis, and gas therapy, achieved a remarkable tumor inhibition rate of ∼75% in a CT26 xenograft model and potently suppressed CT26 cell viability to below 20% at 72 h, showcasing significant suppression of CRC. This study provides an innovative nano-carrier-based synergistic strategy to overcome the current therapeutic bottlenecks in CRC treatment. - Source: PubMed
Publication date: 2026/07/27
Li ChongLiu WeiLi NingfuZhang YanyanWu KeYu Shaohong - Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a five-year survival of approximately 6% that is largely driven by cancer stem cells (CSCs), which promote resistance, metastasis, and recurrence. Mutations in the Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (K-RAS) are common in human PDAC and activate the rat sarcoma (RAS) pathway, thus supporting tumour growth, maintenance, and metastasis. Newcastle Disease Virus (NDV) is a tumour-selective oncolytic virus with a strong safety profile that targets cancer cells and therapy-resistant CSCs, thereby highlighting its potential as an anticancer virotherapy. This study examines NDV AF2240's ability to target CSCs through RAS pathway modulation and apoptosis induction. - Source: PubMed
Publication date: 2026/02/28
Ghasemi Seyed AbbasLing King-HwaIsmail SailaChau De-MingSekawi Zamberi - Prostate cancer kills ≈350,000 yearly. While localized cases have 99% five-year survival, metastatic prostate cancer is hard to treat, with few options for tumors resistant to androgen deprivation. To leverage the immune system to fight prostate cancer, we developed a non-integrative lentiviral vector, namely "Lenti-PROST-02", which encodes clusters of T cell immunodominant regions of human prostatic acid phosphatase and prostate-specific antigen. Immunotherapy with Lenti-PROST-02 in a preclinical virulent prostate tumor model resulted in complete tumor eradication in vast majority of the treated animals. This antitumor effect was concomitant with induction of poly-functional CD8 T splenocyte effectors against numerous T cell epitopes of the antigens encoded by Lenti-PROST-02, increased proportions of tumor-infiltrating CD8 T cells with activated/differentiated/effector phenotype and a "cold-to-hot" inflammatory switch of the tumor microenvironment. Immunity induced by Lenti-PROST-02 was long-lasting and prevented tumor relapse. It was characterized by the persistence of CD44 CD62L CD127 KLRG1 CD8 memory T cells in secondary lymphoid organs, as well as an antigen-diversified memory response. Therefore, Lenti-PROST-02 therapeutic vaccine is a promising approach for prostate immuno-oncotherapy. - Source: PubMed
Publication date: 2026/07/18
Vesin BenjaminFert IngridCiret SylvainDouguet LaëtitiaMoncoq FannyNoirat AmandineAuthié PierreLe Chevalier FabienNevo FabienBlanc CatherineNemirov KirillMajlessi LalehCharneau Pierre