Cdc6
- Known as:
- Cdc6
- Catalog number:
- MA1019
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- SDlabs
- Gene target:
- Cdc6
Related genes to: Cdc6
- Gene:
- CDC6 NIH gene
- Name:
- cell division cycle 6
- Previous symbol:
- CDC18L
- Synonyms:
- -
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-06
- Date modifiied:
- 2019-04-23
Related products to: Cdc6
Related articles to: Cdc6
- Ultra-high dose rate FLASH radiotherapy can mitigate normal tissue toxicity while sustaining tumor control, yet the associated molecular mechanisms are still unclear. This study aimed to evaluate the differential DNA damage and transcriptomic responses of MRC-5 cells to FLASH versus conventional (CONV) irradiation. To address this, MRC-5 cells were exposed to X-rays irradiation at either FLASH dose rate or CONV dose rate. γH2AX/phosphorylated 53BP1 immunofluorescence was performed to detect early-stage DNA double-strand breaks. Transcriptome sequencing was implemented to characterize the transcriptomic expression profiles of the cells. Interaction patterns among differentially expressed genes (DEGs) were investigated via protein-protein interaction (PPI) network analysis. The expression levels of the screened core DEGs were validated via quantitative real-time PCR (RT-qPCR). Results showed that at high doses (8 Gy and 12 Gy), the FLASH group exhibited significantly fewer early-stage DNA double-strand breaks than the CONV group. Its transcriptomic profile was more analogous to that of nonirradiated cells, with differential regulation in DNA damage response (DDR)-related pathways; 9 core DEGs (CCNA2, CCNB1, CCNB2, RAD51, EXO1, BIRC5, BUB1, CDC6, CDC20) were screened out via PPI network analysis, and RT-qPCR verified that their downregulation was less extensive in the FLASH group relative to the latter. Collectively, X-ray FLASH irradiation alleviates MRC-5 cell damage by regulating DNA double-strand break repair and other DDR-related pathways, along with the nine core DEGs, providing a molecular basis for FLASH radiotherapy's normal tissue protective effect. - Source: PubMed
Publication date: 2026/06/15
Jiang YiWang XiaofengYang ChongkaiWu JiangpingChen YaotianLi JieWang QingZhu Wenkun - Intrauterine adhesions (IUA) are fibrotic scars that impair endometrial regeneration, and compromise fertility. Emerging evidence implicates circular RNAs (circRNAs) in fibrotic remodeling, but it remains unclear how the circRNA landscape and circRNA-associated splicing programs coordinately link uterine contractility, endometrial cell-cycle control, and immune activation in IUA. - Source: PubMed
Publication date: 2026/05/07
Chen YingqingJin JingXiang YingWang YanpingWu ShuangZhan NiXiong MengxinDeng Ali - 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 - Pancreatic cancer remains one of the most aggressive malignancies, characterized by early metastatic spread and intrinsic resistance to chemotherapy, which ultimately results in poor treatment outcomes. While the Cell Division Cycle 6 (CDC6) protein has been extensively characterized across multiple cancer types, its functional role in the pathogenesis of pancreatic cancer remains poorly understood. In this study, we performed bioinformatics analysis using RNA-seq data from The Cancer Genome Atlas (TCGA) pancreatic adenocarcinoma cohort, and identified differentially expressed genes through microarray profiling. We conducted a comprehensive functional characterization of CDC6 using CCK-8, colony formation, wound healing, Transwell assays, and flow cytometry, and assessed cellular glycolysis levels based on measurements of ATP production, lactic acid generation, and glucose content. Subcutaneous xenograft mouse models were established to evaluate the impact of CDC6 on tumor growth in vivo, while mechanistic investigations were carried out using co-immunoprecipitation, chromatin immunoprecipitation, dual-luciferase reporter assays, and nucleocytoplasmic fractionation. Our results revealed that CDC6 expression is upregulated in pancreatic cancer, and its elevated expression is significantly correlated with unfavorable patient prognosis. Functional experiments demonstrated that CDC6 promotes the proliferation, migration, and invasion of pancreatic cancer cells. Thrombospondin 1 (THBS1) was identified to be positively correlated with CDC6 expression, and differentially expressed genes were notably enriched in the glucose metabolism pathway. Mechanistically, CDC6 cooperates with E2F1 to facilitate the transcription of THBS1, and the AKT signaling pathway is activated via the CDC6/THBS1 interaction. Overexpression of CDC6 significantly promoted glycolysis and tumor progression in pancreatic cancer, whereas these pro-tumor effects were markedly abrogated by THBS1 knockdown. Collectively, our findings demonstrate that CDC6/THBS1/AKT signaling drives glycolysis and accelerates pancreatic cancer progression, suggesting that the CDC6/THBS1/AKT axis may serve as a promising therapeutic target for pancreatic cancer. - Source: PubMed
Publication date: 2026/04/21
Yin MengqiuChen XiLiu ZiyuWang ChongyuChen TianyuZhu Jinhui - [This corrects the article DOI: 10.3389/fonc.2026.1741406.]. - Source: PubMed
Publication date: 2026/03/04
Shi YiChen FangfangWeng YuanyuanZeng HangChen Gang