CD44 Biotin
- Known as:
- CD44 Biotin
- Catalog number:
- ANT-294
- Product Quantity:
- 500µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- CD44 Biotin
Related genes to: CD44 Biotin
- 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 Biotin
Related articles to: CD44 Biotin
- CD44 is a cell-surface glycoprotein frequently overexpressed in cancers and associated with poor prognosis. We evaluated the prognostic significance of CD44 overexpression in multiple myeloma (MM) and investigated the therapeutic efficacy of combining natural killer (NK) cell therapy with all-trans retinoic acid (ATRA) and bortezomib (Bor) against CD44-overexpressing MM. Clinical data from the CoMMpass database were analyzed to assess survival outcomes relative to CD44 expression. NK cells were expanded from healthy donors using K562-OX40L-mbIL-18/21 feeder cells supplemented with interleukin (IL)-2 and IL-15. Functional assays were performed using CD44-high myeloma cell lines treated with ATRA and Bor, individually or in combination with NK cells. Therapeutic efficacy was evaluated based on tumor growth, systemic dissemination, and survival in an intravenous U266-green fluorescent protein-firefly luciferase xenograft NOD/SCID IL-2Rγnull mouse model. Clinical data showed CD44 overexpression correlated with inferior overall survival (P < 0.0001) in all three stages I, II, and III of the revised International Stage System. In vitro, ATRA and Bor co-treatment downregulated β-catenin and CD44 expression, inhibited proliferation, migration, and invasion, and enhanced NK cell-mediated cytotoxicity via upregulation of MICA/B, Fas, TRAIL-R2, and intercellular adhesion molecule-1. In vivo, combination therapy with NK cells, ATRA, and Bor significantly suppressed CD44 expression, reduced extramedullary spread, and prolonged survival without notable toxicity. These preclinical findings support CD44 overexpression as a marker associated with inferior survival in MM and provide a rationale for pharmacologic tumor priming with ATRA and bortezomib to enhance NK cell-mediated cytotoxicity. However, the therapeutic strategy requires further validation in heterogeneous patient-derived models and prospective clinical studies before clinical efficacy can be inferred. - Source: PubMed
Publication date: 2026/05/21
Nguyen Van-TanThi Thuy NguyenTran Van-Dinh-HuanVo Manh-CuongChu Tan-HuyJang Ho CheolKim MiheeSong Ga-YoungAhn Seo-YeonAhn Jae-SookYang Deok-HwanKim Hyeoung-JoonCho DuckLee ChanghoJung Sung-HoonLee Je-Jung - Lung cancer stem cells (LCSCs) are closely linked to lung cancer progression and drug resistance, and are regulated by the inflammatory microenvironment, such as NLR family pyrin domain containing 3 (NLRP3) inflammasome. Feiyanning (FYN) is a Traditional Chinese Medicine with therapeutic potential for lung cancer. However, its mechanism remains elusive. This study aimed to investigate whether FYN suppresses lung cancer progression by modulating LCSCs and the NLRP3 inflammasome. - Source: PubMed
Publication date: 2026/05/18
Wang ShuangWang LifangSu WanLu YeyunXu Zhenye - One of the leading causes of poor prognosis in colorectal cancer (CRC) patients is the presence of colorectal cancer-initiating cells (CCICs). The tumor microenvironment (TME) plays a role in the acquisition of CCICs characteristics. However, the underlying mechanisms remain unclear. - Source: PubMed
Publication date: 2026/05/20
Liu JingwenXu WeimingPan TianhuiXu LiyiWang RuiMa Minjun - Subretinal fibrosis (SRF) is a critical end-stage feature of neovascular age-related macular degeneration (nAMD) with limited treatment options. However, the pathological mechanism during the transformation of choroidal neovascularization (CNV) into SRF remains unclear. - Source: PubMed
Publication date: 2026/05/19
Lin RuoyiCai ZixinZheng TianyuWu YanXu ZihangLuo YunhongLiang FengZhu ManhuiYu JingCai Wenting - Bladder Cancer (BC) remains a major global health concern due to its high recurrence rate and limited availability of effective targeted therapies. Although gene therapy has emerged as a promising strategy, its clinical translation is hindered by the lack of safe and efficient delivery systems. This research aims to develop a dual-functional nanoparticle system for targeted gene delivery and enhanced therapeutic efficacy. Chitosan-Hyaluronic Acid Dialdehyde nanoparticles (CS-HAD NPs) were synthesized via controlled oxidation and covalent conjugation, enabling CD44 receptor-targeted delivery of Bcl-2 siRNA combined with near-infrared (NIR)-induced photothermal therapy. The optimized nanoparticles exhibited uniform size distribution, high siRNA encapsulation efficiency, and excellent colloidal stability. In vitro cellular assays demonstrated significant reductions in cell viability and Relative Growth Rate (RGR%), with the combined Bcl-2 siRNA@CS-HAD + NIR treatment showing maximum suppression over 24-72h. Western blot and RT-qPCR analyses confirmed effective downregulation of Bcl-2 expression at both protein and mRNA levels. Hemocompatibility markers, including Prothrombin Time (PT), Activated Partial Thromboplastin Time (APTT), Thrombin Time (TT), fibrinogen, Platelet Activation Marker (CD62P expression), and Complement Activation Marker (C3a level), remained within normal physiological ranges, indicating good blood compatibility. These findings demonstrate that the proposed dual-therapy system offers a synergistic anti-cancer effect through targeted gene silencing and photothermal action. The integration of CD44-targeted delivery with combined gene and photothermal therapy using a biocompatible nanoplatform presents a promising and safe approach for bladder cancer treatment, with significant potential for future biomedical applications. This research is limited to in vitro validation. - Source: PubMed
Publication date: 2026/05/19
Liang XinSun YimingGuo YuanyuanLiu BeibeiGu YuchenGao Wuyue