Ask about this productRelated genes to: CDT1 antibody
- Gene:
- CDT1 NIH gene
- Name:
- chromatin licensing and DNA replication factor 1
- Previous symbol:
- -
- Synonyms:
- DUP, RIS2
- Chromosome:
- 16q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-05-25
- Date modifiied:
- 2014-11-19
Related products to: CDT1 antibody
Related articles to: CDT1 antibody
- Emerging data indicate that chromatin licencing and DNA replication factor 1 (CDT1) plays an important role in several cancers. However, it remains unclear whether CDT1 is functionally indispensable in lung cancer. Here, constructing tissue microarrays and performing in vitro and vivo experiments, we showed that CDT1 was significantly overexpressed in lung adenocarcinoma tissues, and its expression level significantly correlated with pathological stage, tumour invasiveness, and overall patient survival. Mechanistic investigations revealed that CDT1 possibly interacted with the transcription factor adenovirus early region 2 binding factor 1 (E2F1), thereby cooperatively enhancing the transcriptional activity of the targeting protein for Xenopus kinesin-like protein 2 (TPX2) gene. This phenomenon subsequently increased the expression of glycolysis-related molecules aldolase C and pyruvate kinase M2 via the PI3K/AKT signalling pathway, which promoted the proliferation and migration of non-small cell lung cancer (NSCLC) cells. Critically, knockdown of TPX2 or treatment with either the AKT pathway inhibitor MK-2206 2HCl or the glycolysis inhibitor AZ33 effectively reversed the promoting effects of CDT1 on AKT pathway activity, glycolytic metabolism, and tumour progression in CDT1-overexpressing NSCLC cells. Collectively, this study elucidates that CDT1 and E2F1 mutually promote the glycolysis and progression of NSCLC cells by activating the TPX2/AKT pathway. These findings provide novel therapeutic targets for refractory NSCLC treatment. - Source: PubMed
Publication date: 2026/04/24
Tan JianfengZhu LeqingHu BangxianWang ZiyiZhang JianhuaGuo QuanweiKuang JunYan JunMo YijunZheng QingyouWu YonghuiYang Yinggui - The inference of molecular information from hematoxylin-eosin (HE) specimens may reduce the ancillary testing burden in digital pathology. - Source: PubMed
Publication date: 2026/04/25
Urata TakumiTakeyama SaoriKimura FumikazuOhshima KengoIshii KeikoJi CunyuanTakagi GenYamaguchi Masahiro - In colorectal cancer liver metastases, chromosomal instability (CIN) serves as a critical hallmark linked to tumor aggressiveness and poor prognosis. This study integrated single-cell RNA sequencing, weighted gene co-expression network analysis, and non-negative matrix factorization to construct a comprehensive CIN index, revealing that CIN-high tumor cells exhibit more aggressive phenotypes and reside in an immune-excluded tumor microenvironment. Cancer-associated fibroblasts (CAFs) showed enhanced communication with CIN-high tumor cells, and a key CAF-derived gene, CCDC3, was experimentally validated to promote metastasis, proliferation, and CIN in vitro and in vivo. The bio-knowledge graph analysis based on artificial intelligence further revealed the core regulation of CCDC3 in chromosomal instability and liver metastasis of colorectal cancer. Mechanistically, CCDC3 physically interacts with CXCR3 on CRC cells, activating STAT3 phosphorylation and subsequent CDT1 transcription, forming a CCDC3/CXCR3/STAT3/CDT1 signaling axis. Disruption of this axis-either by genetic knockdown or pharmacological inhibition-significantly suppressed metastatic traits, tumor growth, and liver colonization in mouse models. Clinically, high CCDC3 expression correlated with elevated CIN signatures and worse patient survival. These findings uncover a novel CAF-driven signaling pathway that promotes CIN and metastatic progression in CRC, highlighting its potential as a therapeutic target for aggressive, CIN-high colorectal cancer. - Source: PubMed
Publication date: 2026/03/07
Huang RunzeLiu QinyuJin XinBai XuanciWu YibinHe XiganWang YixiuJiang ZitingZhang YongfaShi YiWang LuZhu Weiping - Chromatin loading of the hexameric replicative helicase MCM2-7 complex requires coordinated interactions with the origin recognition complex (ORC), CDC6, and CDT1. MCM2-7 not bound to DNA forms a single hexamer (SH) with an open DNA entry gate between MCM2 and MCM5. Two MCM2-7 SHs can be loaded sequentially to form the double hexamer (DH) that encircles the DNA duplex. Activated MCM2-7 then unwinds DNA and initiates DNA replication. Our cryoelectron microscopy analyses show that a fraction of human MCM2-7 without DNA exists as DH. Unexpectedly, we find that the MCM3 winged helix domain (WHD) docks on MCM2 in both DNA-free DH and SH, creating a safety latch across the DNA entry gate to block DNA entry into the central channel. The safety latch can be opened by ORC-CDC6 binding. Perturbing this latch by structure-based or disease-related mutations of MCM3 causes replication defects and DNA damage checkpoint activation. Shortening the MCM3 linker between the helicase domain and WHD alleviates the cell cycle defects of the latch-strengthening mutation. Our findings uncover a regulated step in MCM2-7 loading with implications for human diseases. - Source: PubMed
Publication date: 2026/02/20
Liu YusongYang MengquanLu PingGao HaishanHe MaozhouWang YitaoQi AoCao TingZhang QiuqinQi ShutaoShi YigongYu Hongtao - Candida auris is an emerging fungal pathogen notable for its intrinsically high resistance to fluconazole, the most prescribed antifungal drug. However, the genetic regulators underlying fluconazole susceptibility in C. auris remain unclear. Here we performed a pooled screen of piggyBac (PB) transposition mutants and identified significant enrichment of mitochondrial genes whose inactivation reduces fluconazole susceptibility. A genome-wide genetic interaction analysis of a mitochondrial gene deletion mutant, pet309Δ, suggests that the vacuolar calcium pump homologue CDT1 (Calcium and Drug Transporter 1) is responsible for its reduced fluconazole susceptibility. Fluconazole induces significant upregulation of CDT1 through the calcineurin signalling pathway. Cdt1, beyond its canonical calcium-pumping function, has evolved another function in mediating fluconazole efflux through its fluconazole-induced, calcineurin- and ATP hydrolysis-dependent plasma membrane localization. In addition, Cdt1 accelerates the evolution of fluconazole resistance or tolerance, and its transcript levels are substantially elevated across resistant clinical isolates. Our findings reveal a neofunctionalized role for Cdt1 in mediating fluconazole efflux in C. auris. - Source: PubMed
Publication date: 2026/02/17
Song YabingChen JinxinWan JunhuaZhang JiamoLiu QizhengSun FeiZhang HanlinGuo YuruChow Eve W LChen YaliYan ZiyuWang JianbinChen KunWang YueGao Jiaxin