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
- Endocrine-disrupting chemicals (EDCs) are widely present in the environment and consumer products and may disturb thyroid hormone homeostasis. However, the molecular mechanisms linking EDC exposure to thyroid cancer progression remain unclear. This study integrated toxicity prediction, toxicogenomics, transcriptomic analysis, machine learning, molecular simulation, and experimental validation to identify EDC-related key targets in thyroid cancer. ADMETlab 3.0 was used to evaluate the potential toxicity of BPA, PFOA, DDT, BDE-209, TCDD, and DEHP, and compound-related genes were obtained from the CTD database. By integrating thyroid cancer-related genes from multiple disease databases, 1113 shared EDC-thyroid cancer targets were identified and were mainly enriched in PI3K-Akt, FoxO, and AGE-RAGE signaling pathways. Combined with differential expression analysis, machine learning identified a six-gene diagnostic model consisting of FN1, BCL2, CD44, CDKN1A, CTNNB1, and JUN. The Lasso + LDA model achieved an average AUC of 0.976 across the training cohort and three external validation cohorts. CD44 showed robust diagnostic performance, with AUC values of 0.950, 0.801, 0.878, and 0.938 in the training set, GSE27155, GSE29265, and GSE153659, respectively, and had the highest contribution in SHAP analysis. Immune infiltration, TCGA survival, and single-cell analyses indicated that CD44 was associated with the tumor immune microenvironment, cellular state changes, and prognosis. Molecular docking and 200 ns molecular dynamics simulations generated plausible docking poses of BPA, DEHP, and PFOA on CD44, with PFOA showing the most favorable predicted docking score. Experimental validation showed higher CD44 expression in thyroid cancer tissues and cells and increased CD44 expression following EDC exposure. CD44 knockdown attenuated EDC-associated increases in proliferation, colony formation, and migration. These findings identify CD44 as a candidate molecule associated with EDC-responsive malignant phenotypes in thyroid cancer. - Source: PubMed
Publication date: 2026/08/30
Hu YifanLiu KeshuChen TingHe ZhizhenLi ShuangHu WuFu QiuyangChen Xiong - Immune checkpoint inhibitors (ICIs) are first-line therapy for cervical cancer (CC), yet their efficacy is limited to a subset of patients owing to low tumor immunogenicity. Single-cell RNA sequencing revealed that CC patients exhibiting robust immune responses following radiotherapy (RT) showed upregulation of necroptosis along with lower baseline RIPK1 expression. In vitro and in vivo experiments further illustrated that RT alone upregulates RIPK1 expression. Inspired by these findings, we developed a hafnium (Hf)-based nanoscale metal-organic framework loaded with LD4172, a RIPK1 degrader (LD4172/Hf). The combination of RT and LD4172/Hf effectively induced necroptosis, and elicited a potent immune response via triggering necroptosis-mediated immunogenic cell death (NICD). This effect was characterized by enhanced macrophage infiltration and phagocytosis, increased M1 polarization, reduced M2 polarization, and improved antigen presentation capacity in macrophages. Furthermore, combined RT + LD4172/Hf with PD‑1 blockade amplified the anti‑tumor immunity driven by NICD. This combined treatment nearly doubled the production of tumor-killing cytokines (IFNγ and GZMB) in CD8 T cells and promoted the expansion of CD44⁺ effector memory T cells upon tumor rechallenge, compared with RT plus PD-1 blockade alone, thereby enabling efficient tumor elimination and conferring protection against tumor relapse. Collectively, these findings position LD4172/Hf in combination with radio-immunotherapy as a promising therapeutic strategy for CC patients. - Source: PubMed
Publication date: 2026/08/22
Wu TongLv BinWang HanHe GuangpingFu YuandongJi XiuruZeng YulianNi DalongQiu JunjunHua Keqin - Photodynamic therapy (PDT) efficacy is severely compromised by tumor hypoxia and the scarcity of efficient type-I photosensitizers, necessitating multimodal therapeutic strategies. Herein, we report a porphyrin-Cu (II) covalent organic framework (TBCOF) with intrinsic bifunctional photodynamic and chemodynamic activities. Sequential DOX encapsulation and hyaluronic acid (HA) surface functionalization afford HA-TBCOF@DOX, a tumor-targeted nanoplatform integrating four synergistic therapeutic modalities. Under 660 nm laser irradiation, the nanoplatform generates ROS signatures consistent with both type-I and type-II pathways for PDT, while the intrinsic Cu centers are proposed to catalyze a Fenton-like reaction consistent with •OH generation for CDT. Concurrently, observations of O evolution suggest catalase-like activity that may decompose endogenous HO into O, alleviating hypoxia and potentiating oxygen-dependent PDT. Efficient photothermal conversion and pH-triggered DOX release contribute to photothermal and chemotherapeutic effects, respectively, while HA-mediated CD44 targeting enhances cellular uptake and therapeutic specificity. In vitro and in vivo studies demonstrate that laser-activated HA-TBCOF@DOX effectively suppresses tumor growth, induces apoptosis, and exhibits no apparent systemic toxicity under the tested experimental conditions. This work establishes a multifunctional COF-based nanoplatform that addresses PDT limitations observed in this study by integrating intrinsic PDT and CDT, providing a robust strategy for synergistic multimodal cancer therapy. - Source: PubMed
Publication date: 2026/08/17
Mo YongjieHou JieLi HongliWang LijuanZhao LinluZhu LinhuaDai Chunyan - Intervertebral disc degeneration (IVDD) is a common cause of chronic low back pain, imposing a significant economic and physiological burden on individuals and society worldwide. Although dysregulation of the WNT/β-catenin pathway is considered an important factor contributing to the dysfunction of nucleus pulposus (NP) cells and degradation of the extracellular matrix, the mechanisms by which specific subgroups of NP cells are activated and the maintenance of excessive activation of specific pathways remain unclear. - Source: PubMed
Publication date: 2026/08/22
Li QiuweiLiang GuoyanBo KaidaKang LiangJin PeilinZhao ChenhaoZhang RenjieLyu FengjuanShen Cailiang - Chronic non-bacterial prostatitis (CNP), a prevalent and debilitating urological disorder affecting 8.4% of men aged 15-60 years, presents significant clinical challenges due to the paucity of targeted therapies and poor patient adherence. To address this unmet medical need, we developed an innovative multifunctional nanoplatform (QM (Zn) NPs) by integrating TiC MXene with a quercetin-zinc coordination complex (Que-Zn) for precision CNP therapy. This system leverages chondroitin sulfate (Chs)-mediated CD44 targeting to achieve selective accumulation in inflamed prostate tissue, thereby enhancing Zn bioavailability while enabling co-delivery of MXene and Que-Zn therapeutic payloads. Upon localization, QM (Zn) NPs orchestrate a coordinated therapeutic cascade: MXene scavenges reactive oxygen species (ROS) electron-deficient sites, while Que-Zn drives M1-to-M2 macrophage repolarization and facilitates Zn cellular uptake. The accumulated intracellular Zn critically upregulates metallothionein 1 (Mt1), activating the IKK/NF-κB/IκB axis to resolve inflammation and oxidative damage. Transcriptomic analysis unequivocally identified Mt1 as the pivotal mediator of Zn-driven microenvironment reprogramming. Notably, QM (Zn) NPs not only significantly alleviated pelvic pain by mitigating neuronal oxidative stress but also exhibited excellent biocompatibility. This work pioneers a targeted nano-theranostic strategy that synergistically restores zinc homeostasis, quenches ROS, and reprograms immune responses, thereby establishing a transformative paradigm for CNP management. - Source: PubMed
Publication date: 2026/08/21
Liu KailaiZhang YuchenGao YanyaoZheng YunheHuang YuHe JiangchuanWang TingZhou HanchaoWen JinpengSun ZhengyeWang KekeFu QiangSong BinWang HeWang LeiZhang GengWang Ke