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
- Colorectal cancer (CRC) remains a major cause of cancer-related mortality due to therapeutic resistance. Because colorectal cancer stem-like cells (CRCSCs) play a central role in tumor initiation and progression, therapeutic strategies addressing CSC-enriched populations are urgently needed. In this study, we investigated the anticancer effects of emodin, a natural anthraquinone, in CSC-enriched tumorsphere models. Emodin significantly suppressed the viability and self-renewal capacity of HCT116- and SW480-derived CSCs. It induced G0/G1 cell cycle arrest and markedly downregulated stemness-associated markers (CD44, CD133, ALDH1A1, SOX2, NANOG, and OCT4). Importantly, emodin-induced cell death was characterized by mitochondrial dysfunction, increased mitochondrial reactive oxygen species, loss of membrane potential, and nuclear translocation of apoptosis-inducing factor (AIF). This cytotoxicity was not rescued by the pan-caspase inhibitor Z-VAD-FMK, confirming caspase-independent apoptosis. Furthermore, network pharmacology and experimental validation identified GSK3β as a key target. Emodin reduced Wnt/β-catenin signaling by decreasing β-catenin stabilization and nuclear accumulation. Crucially, a rescue experiment utilizing LiCl confirmed that emodin's suppressive effects are mechanistically dependent on the GSK3β/Wnt/β-catenin axis. Collectively, emodin suppresses CRCSC characteristics by downregulating Wnt/β-catenin signaling and inducing AIF-associated caspase-independent apoptosis, highlighting its therapeutic potential against CRC. - Source: PubMed
Publication date: 2026/08/31
Ahmadi MahdiehKim Hong LaeJung Hye Jin - Metastatic spread defines the lethality of cervical cancer (CC). Connective tissue growth factor (CTGF/CCN2) regulates cell- extracellular matrix interactions but its role in CC is not well-defined. This study investigates the role of CTGF in driving CC invasive growth and its prevalence in patient tissues. - Source: PubMed
VON DER Brelie LindaKalyoncu Nesibe GökçeGallwas JuliaGründker Carsten - Microsatellite-stable (MSS) colorectal cancer (CRC) generally responds poorly to immune checkpoint blockade, but some MSS tumors are T-cell rich. We examined whether such infiltration reflected effective immunity or functional immune constraint. - Source: PubMed
Liu WenxuZheng YipanWang HaoQi FengZhao XiulanMa ZhenyiLiu Zhe - Persistent activation of the Notch signaling pathway is closely associated with the maintenance of cancer stem cells (CSCs) and the progression of hepatocellular carcinoma (HCC). Recombination signal binding protein for immunoglobulin kappa J region (RBPJ), a key transcription factor that mediates downstream target gene transcription in the Notch pathway, has not been fully characterized with respect to its role in promoting CSC traits in HCC. In this study, we found that RBPJ is markedly upregulated in HCC and is associated with selected clinicopathologic features. RBPJ also promoted stem-like phenotypes in HCC cells. Mechanistically, TRIM41 interacts with RBPJ and mediates K63-linked polyubiquitination of RBPJ at Lys135, thereby stabilizing RBPJ and enhancing RBPJ-mediated transcriptional activation of the stemness-related genes SOX2 and CD44. Consequently, the TRIM41-RBPJ axis sustains CSC-like properties in HCC cells. Our findings identify a previously unrecognized post-translational mechanism by which TRIM41-mediated stabilization of RBPJ promotes stem-like properties. These findings expand our understanding of the post-translational regulation of RBPJ in HCC and highlight the TRIM41-RBPJ axis as a potential molecular target warranting further investigation. - Source: PubMed
Publication date: 2026/08/31
Wu HaoWu JinqiaoZhang XinyuYao YuxinYe DongjieZhang ZhuYang HaoyiWang XiaoqianTang Nanhong - Acute-on-chronic liver failure (ACLF) is a fatal syndrome defined by hepatic decompensation and systemic inflammation, yet the underlying cellular networks remain elusive. Here, we established an ACLF mouse model recapitulating clinical hallmarks and performed single-cell RNA sequencing (scRNA-seq) on hepatic non-parenchymal cells (NPCs). We identified 30 cell clusters and observed profound spatial remodeling of NPCs driven by pro-inflammatory mediators. Endothelial cells (ECs) underwent a critical transition from homeostasis to dysfunction, marked by mitochondrial damage and activation of NF-κB and MAPK pathways. Ligand-receptor interactome analysis identified dysfunctional ECs as central hubs driving global network reconfiguration, primarily via the Lgals9-Ighm/Cd45/Cd44 axes, alongside the suppression of homeostatic signals (Cd55 and APP). Furthermore, we mapped B cell lineage trajectories and validated the spatial co-localization of EC and B-cell interactions through Lgals9-Ighm. This study defines the EC and B-cell communication landscape and suggests that the Lgals9-Ighm axis may play a critical role in ACLF progression, representing a potential candidate for therapeutic intervention. - Source: PubMed
Jia JieDong YuehongZhao YuLi ShaoyouMou Tangwei