Ask about this productRelated genes to: NDRG1 Blocking Peptide
- Gene:
- NDRG1 NIH gene
- Name:
- N-myc downstream regulated 1
- Previous symbol:
- CAP43
- Synonyms:
- DRG1, RTP, TDD5, NDR1
- Chromosome:
- 8q24.22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-23
- Date modifiied:
- 2019-04-23
Related products to: NDRG1 Blocking Peptide
Related articles to: NDRG1 Blocking Peptide
- Cancer cells exploit DNA repair to overcome damage and errors induced by rapid proliferation and repressed checkpoints. Thus, the loss of one DNA repair protein can make tumors more susceptible to inhibition of other repair pathways. Here, using in silico methodologies and high-content genetic and cell survival screens, we found that the antimalarial drug quinacrine impaired the DNA damage response (DDR) in multiple cancer cell lines. Quinacrine disrupted the interaction of the stress-response protein NDRG1 with the major segregase VCP, which in turn promoted the degradation of the E3 ubiquitin ligase RNF8 and other proteins that mediate the recruitment of the critical DDR protein 53BP1 to sites of DNA damage. This impaired recruitment of 53BP1 caused increases in the DNA damage marker γH2AX. High expression in tumors correlated with poor survival in patients, and high expression in various cancer cell lines correlated with quinacrine sensitivity. Colorectal carcinoma cells were particularly vulnerable to pharmacological or genetic inhibition of NDRG1, and high expression and mutations in and resulted in synthetic lethality. Our findings identify combination genetic markers that might be therapeutically exploited in colon cancer, as well as provide a platform for such discovery in distinct cancer types. - Source: PubMed
Publication date: 2026/07/21
Mkrtchyan Garik VVeviorskiy AlexanderMeisen Zarah GPetr Michael AMercurio Tobias ClausenBakula DanielaSykora PeterKuo Li-WeiRosenthal Dean SSimbulan-Rosenthal Cynthia MZhang PeiranTang QiuqiongOsipov Andreyan NOzerov Ivan VAliper AlexZhavoronkov AlexScheibye-Knudsen Morten - High-grade serous ovarian cancer (HGSOC) exhibits profound immunologic and metabolic remodeling, yet the macrophage programs that drive disease progression and therapeutic resistance remain incompletely defined. Here, we integrate spatial transcriptomics, single-cell sequencing, bulk deconvolution, pseudotime reconstruction, and multiplex immunofluorescence to delineate a distinct tumor-promoting macrophage phenotype, termed Macro4, characterized by hypoxia adaptation, extracellular matrix remodeling, and pro-angiogenic signaling. Macro4 signature-based RSF model robustly predicted poor survival across multiple cohorts and remained an independent prognostic factor when combined with clinical variables. Mechanistically, Macro4 macrophages displayed strong VEGF- and SPP1-mediated communication with endothelial cells and occupied hypoxic, angiogenesis-enriched niches. Trajectory inference revealed that Macro4 arises from an inflammatory lineage that transitions toward glycolytic and matrix-remodeling terminal states under microenvironmental stress. Among Macro4-enriched genes, NDRG1 emerged as the dominant regulator, selectively expressed within Macro4, enriched across hypoxia-related pathways, associated with adverse overall survival in Cox analysis, and linked to chemoresistance and shorter progression-free survival. Spatial and protein-level validation confirmed that NDRG1⁺SPP1⁺ macrophages form discrete angiogenic niches and are preferentially localized to primary tumor sites. Together, our findings identify NDRG1+ Macro4 macrophages as a hypoxia-driven angiogenic niche associated with macrophage remodeling and platinum resistance in HGSOC, providing a framework for future macrophage-targeted therapeutic studies. - Source: PubMed
Publication date: 2026/07/13
Bu LanyingDing ZiyangRen ZhangqiZhao RuihengZhou YingZhou Hong - Tamoxifen is a key endocrine therapy for estrogen receptor-positive (ER) breast cancer, but acquired resistance limits long-term efficacy. The molecular mechanisms remain complex, and predictive biomarkers are lacking. Gene expression data related to tamoxifen resistance were obtained from GEO (GSE67916), and differentially expressed genes (DEGs) were identified using the limma algorithm. Functional enrichment analyses (GO and KEGG) revealed involvement in immune processes, antiviral responses, endocytosis, lysosome pathways, and estrogen signaling. Three machine learning algorithms (LASSO, SVM-RFE, and RF) identified six hub genes (CAMK1D, CHAC1, KIAA0513, MED13, NDRG1, STXBP5). A prognostic risk model based on these genes was constructed using TCGA-BRCA data, effectively stratifying patients into high- and low-risk groups with significantly different overall survival. The model demonstrated good predictive accuracy (AUC = 0.70) and stable performance in time-dependent ROC analyses, validated in an independent cohort. This study provides a robust tamoxifen resistance-related gene signature and a multigene prognostic model, offering novel insights into resistance mechanisms and potential guidance for individualized prognosis and therapy in ER breast cancer. - Source: PubMed
Publication date: 2026/06/26
Gao ChaoxuShi GuojianHou LiliLi LingWang WeijieLi XiaohuaLiu Song-Bai - Senescence-related transcriptional programs and epithelial-mesenchymal transition (EMT) are implicated in pancreatic ductal adenocarcinoma (PDAC) progression and therapy resistance. However, the single-cell distribution, functional heterogeneity, and clinical relevance of EMT-associated senescence-like programs remain incompletely defined. - Source: PubMed
Publication date: 2026/07/08
Chen Long-JiangWu LunChen Su-HangPan XuanShen Zheng-ChaoWang JieZhang ShuoZhai Lu-LuWang Xiao-Ming - As a first-line treatment for EGFR-mutated non-small cell lung cancer (NSCLC), acquired resistance to osimertinib has become a major clinical challenge. Traditional two-dimensional cell culture models have significant limitations in simulating the tumor microenvironment, making it difficult to fully elucidate complex resistance mechanisms. In recent years, three-dimensional organoid models have emerged as a crucial platform for studying resistance mechanisms due to their superior ability to preserve tumor tissue architecture and heterogeneity. Angiopoietin-like protein 4 (ANGPTL4), a secreted glycoprotein, has been implicated in regulating extracellular matrix remodeling and is associated with chemotherapy resistance in multiple cancers. However, its specific role in osimertinib resistance remains unclear. Therefore, this study investigates the mechanism of ANGPTL4 in lung cancer resistance using organoid models. - Source: PubMed
Publication date: 2026/07/07
Zhou Dai-YanXie PeiWang Si-YuanLiu Wei-LuHao Meng-DiWang Zi-YiZeng Xin-XinZhang Xu-Hui