Ask about this productRelated genes to: CUEDC1 Blocking Peptide
- Gene:
- CUEDC1 NIH gene
- Name:
- CUE domain containing 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17q22
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-04
- Date modifiied:
- 2016-10-05
Related products to: CUEDC1 Blocking Peptide
Related articles to: CUEDC1 Blocking Peptide
- CUE domain containing protein 1 (CUEDC1) is implicated in tumor progression; however, its specific role in esophageal cancer (ESCA) remains unclear. In esophageal cancer, the expression of CUEDC1 is notably low, which correlates with reduced survival rates and adverse clinical outcomes. Overexpression of CUEDC1 results in decreased activity of the JAK1/STAT3 signaling pathway in cells, consequently diminishing their proliferation, migration, and invasion capabilities. This mechanism operates through the direct binding of CUEDC1 to STAT3, facilitating its ubiquitination and triggering the ubiquitin-proteasome degradation pathway, ultimately leading to a significant reduction in intracellular STAT3 levels. This study suggests that CUEDC1 can reduce intracellular STAT3 protein levels, thereby inhibiting JAK1/STAT3 signaling transduction and suppressing the progression of ESCA. This study aims to elucidate the regulatory mechanism of CUEDC1 on STAT3, which will enhance our understanding of the regulatory pathways involved in the treatment of esophageal cancer and potentially other tumors. Future breakthroughs and innovations may emerge from molecular research and development targeting this pathway. - Source: PubMed
Publication date: 2026/03/31
Li ZhuoPan ZhipengSu XuehanLi ChunhongZhang JianLin GuoheLi HaowuCui YueXuan Han - BACKGROUND: The reprogramming of energy metabolism, particularly glycolysis, upholds the malignancy of tumors. The relationship between CUE domain-containing protein-1 (CUEDC1) and glycolysis, along with its influence on the development of estrogen receptor-positive breast cancer (ER+ BRCA), is not well defined. This investigation explores the functional involvement of CUEDC1 in glycolysis regulation and uncovers a previously unidentified pathway contributing to the progression of ER+ BRCA. METHODS: Immunohistochemistry, western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were used to detect the expression of CUEDC1 in ER+ BRCA tissues and cell lines. A series of molecular analyses, including dual-luciferase reporter assays, RNA-seq, and chromatin immunoprecipitation (ChIP), were performed to elucidate the potential mechanisms underlying CUEDC1’s involvement in ER+ BRCA progression. Metabolic assays focusing on glycolysis were employed to investigate the functional roles of CUEDC1 and calcium voltage-gated channel auxiliary subunit gamma 4 (CACNG4). The Connectivity Map (CMap) database was utilized to screen CUEDC1 inhibitors. RESULTS: CUEDC1 is aberrantly upregulated in ER+ BRCA tissues and cells. Increased CUEDC1 can promote enhanced tumor growth and lead to poor clinical outcomes in patients with ER+ BRCA. The MYC associated zinc finger protein (MAZ) can upregulate CUEDC1 gene transcription in ER+ BRCA cells by directly binding to its promoter. We determined that CUEDC1 directly modulated CACNG4 to enhance phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway activation, thereby facilitating tumor growth of ER+ BRCA. Clinical observations also revealed a positive correlation between CACNG4 expression and CUEDC1, with both factors being strongly associated with poor prognosis in patients with ER+ BRCA. Mechanistically, The CUEDC1/CACNG4/PI3K signal axis enhanced glycolysis through upregulating glucose transporter 1 (GLUT1), a crucial protein in glucose metabolism, thereby supporting tumor growth of ER+ BRCA. Furthermore, methotrexate was identified as a potential inhibitor of CUEDC1. Importantly, the combination of ipatasertib (a PI3K/AKT pathway inhibitor), with methotrexate effectively suppressed growth of ER+ BRCA in a mouse model. CONCLUSIONS: Our research reveals that enhanced CUEDC1 plays an essential role to ER+ BRCA cell proliferation and tumor growth via the CACNG4/PI3K axis. CUEDC1 is a promising prognostic factor of ER+ BRCA, and the CUEDC1/CACNG4/PI3K axis can serve as a potential therapeutic target for ER+ BRCA treatment. - Source: PubMed
Publication date: 2025/11/28
Lu ZexiuLei MingChen JianDeng AoChang ChaoChen JingMeng DieWang RuiWan XueyingTu GangLiu ManranTang Lingfeng - Human epidemiological studies have statistically localized a multitude of quantitative trait loci (QTLs) for blood pressure (BP). However, their potential pathogenic mechanisms causing hypertension remain mysterious. To fill this void, we utilized congenic knock-in genetics to physiologically analyze the BP effects of individual and combinational QTLs. The effect magnitude from a single QTL in vivo ranged from 33.8 to 59.8%. 'Double' and multiple combinations of QTLs exhibited the same BP impact as a single QTL alone. Consequently, the products of these QTLs seemed to belong to the same pathway involved in physiological BP regulations. From this, we identified a novel pathway of hypertension pathogenesis in vivo controlled by the CUE domain containing 1 protein (Cuedc1). This pathway physiologically modulates blood pressure, aldosterone production, and renal and cardiac functions. CUEDC1 originated from common mammalian ancestors, partly explaining similar blood pressures between humans and rodents on this shared mechanistic basis. A translation of CUEDC1 into diagnostic and treatment applications to humans seems individualized and mechanistic because humans and rats may utilize the same BP-regulating mechanisms involving CUEDC1. The future sustainability of post-GWAS will depend on a balanced and robust 'ecosystem' provided by model studies that are founded on the physiologies and mechanisms of BP regulations in vivo. - Source: PubMed
Publication date: 2025/04/17
Deng David WMénard AnnieDeng Alan Y - To explore the precise molecular by which CUEDC1, a 42 kDa protein containing a CUE domain located on chromosome 17q22, contributes to liver cancer metastasis. - Source: PubMed
Publication date: 2025/02/11
Zhou AngjianChen FuyuChen Zhongchao - Hepatic carcinoma is one of the most common types of malignant tumors in the digestive system, and its biological characteristics determine its high rate of metastasis and recurrence after radical resection, leading to a poor prognosis for patients. Increasing evidence demonstrates that phosphoproteins and phosphorylation-mediated molecular pathways influence the occurrence and development of hepatic carcinoma. It is urgent need to develop early-stage biomarkers for improving diagnosis, therapy, medical service, and prognostic assessment. We hypothesize that phosphoproteome and phosphorylation-mediated signaling pathway networks significantly differ in human early-stage primary hepatic carcinomas relative to control liver tissues, which will identify the key differentially phosphorylated proteins and phosphorylation-mediated signaling pathway network alterations in human early-stage primary hepatic carcinoma to innovate predictive diagnosis, prognostic assessment, and personalized medical services and progress beyond the state of the art in the framework of predictive, preventive, and personalized medicine (PPPM). - Source: PubMed
Publication date: 2023/08/10
Zhang YupingLi NaYang LameiJia WenshuangLi ZhijunShao QianwenZhan Xianquan