CDC25C
- Known as:
- CDC25C
- Catalog number:
- 000207A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CDC25C
Related genes to: CDC25C
- Gene:
- CDC25C NIH gene
- Name:
- cell division cycle 25C
- Previous symbol:
- CDC25
- Synonyms:
- PPP1R60
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-06
- Date modifiied:
- 2017-12-06
Related products to: CDC25C
Related articles to: CDC25C
- Benzo(a)pyrene (BaP), an environmental carcinogen, contributes to colon cancer pathogenesis through incompletely elucidated mechanisms. This study integrated network toxicology and multi-omics analyses to decipher BaP-associated molecular signatures and clinical relevance in colon cancer. Using TCGA-COAD data, 113 differentially expressed BaP-related targets were identified via CTD and Super-PRED databases. PPI networks, functional enrichment, and Cox/Lasso regression revealed key pathways (xenobiotic metabolism, p53 signaling, cell cycle) and six prognostic genes (CLK2, CRYAB, RPS6KA1, DPP7, CDC25C, GAST). A BaP-related risk model stratified patients into distinct survival groups. A nomogram accurately predicted 1-, 3-, and 5-year overall survival. High-risk scores correlated with advanced tumor stage, metastasis, and immunosuppressive microenvironments. Molecular docking demonstrated strong BaP binding to CLK2 and CRYAB. External validation (GSE39582, TNMplot) confirmed tumor-specific gene expression patterns. These findings delineate BaP-driven networks connecting xenobiotic stress, immune dysregulation, and tumor progression. The risk model provides a prognostic biomarker for personalized management and therapeutic targeting in colon cancer. - Source: PubMed
Publication date: 2026/04/22
Yang XueyingYang ZhendongSui Bowen - The splicing kinase family contributes significantly to tumor progression. As a member of this family, PRPF4B has been directly implicated in oncogenic processes. However, little is known about the precise role and underlying mechanisms of PRPF4B in hepatocellular carcinoma (HCC). In this study, we found that the expression of PRPF4B was upregulated and associated with a poor prognosis in HCC patients. PRPF4B knockdown significantly suppressed HCC cell proliferation, migration, and invasion while concurrently inducing apoptosis. Knockdown of PRPF4B induced DNA damage via reactive oxygen species (ROS) accumulation, leading to cell cycle arrest at the G2/M phase. This arrest was associated with increased phosphorylation of CDC2, elevated γ-H2AX levels, and downregulation of CDC25C and cyclin B1. In addition, we found that expression of PRPF4B was upregulated in sorafenib no-responders (NR) compared with sorafenib responders (R). PRPF4B knockdown sensitizes HCC cells to sorafenib treatment. Mechanistically, we demonstrated that knockdown of PRPF4B inhibited HCC proliferation through NF-κB pathway. Furthermore, PRPF4B interacts with TIA1. Knockdown of PRPF4B promotes the expression of a specific TIA1 splice variant, leading to altered mRNA splicing that inhibits NF-κB activity. Our findings reveal that PRPF4B interacts with TIA1 and modulates its splicing. Knockdown of PRPF4B triggers ROS-dependent DNA damage, cell cycle arrest, and suppression of HCC proliferation, while enhancing sorafenib sensitivity via inhibition of the NF-κB pathway. Therefore, PPRF4B may be a potential therapeutic target for HCC treatment and sorafenib sensitization. - Source: PubMed
Publication date: 2026/04/01
Zhang CanxueHuang ZhihongSu YutingLiu YuqiZhang ChiGe ChaoTian WeiYang YueTian Hua - Oral squamous cell carcinoma (OSCC) is a common malignancy. Isoliensinine, a bisbenzylisoquinoline alkaloid from , exhibits diverse biological activities, but its microRNA-mediated regulation of the MAPK pathway in anti-OSCC remains unreported. Therefore, this study took OSCC cell lines HSC-3 and HSC-4 as research objects to explore the biological activity and the molecular mechanism of isoliensinine on OSCC. The CCK-8 results revealed that isoliensinine inhibited the proliferation of HSC-3 and HSC-4 cells in a time and drug concentration-dependent manner. Analysis of mRNA and small RNA sequencing revealed that isoliensinine induced significant differences in the expression of 1878 genes and 77 microRNAs (miRNAs) in HSC-3 cells. The GO and KEGG analyses of these differentially expressed genes and miRNAs unveiled their potential role in modulating MAPK signaling. Flow cytometry analysis demonstrated that isoliensinine significantly increased reactive oxygen species (ROS) levels, reduced mitochondrial membrane potential (MMP), induced apoptosis, and caused G2 phase arrest in HSC-3 and HSC-4 cells. Western blot results indicated that isoliensinine upregulated the expression of p-p38, p-SAPK/JNK, p-cdc2, p-cdc25C, Bax, cleaved caspase-9/-3, and cleaved PARP, and downregulated the expression of p-ERK1/2, Bcl-2, and Cyclin B1 in HSC-3 and HSC-4 cells. The results demonstrate that isoliensinine induces apoptosis in OSCC cells via ROS-mediated mitochondrial pathways and cell cycle arrest, a process associated with MAPK signaling pathway activation. Transcriptome analysis further revealed that isoliensinine modulates multiple miRNAs that target the MAPK pathway, suggesting that miRNA regulation may mediate its activation of MAPK signaling. - Source: PubMed
Publication date: 2026/02/15
Cai Zi-WeiZhao WeiGong Yu-PingZhou Yi-ChuanPu Shi-QiBai Xiao-YuLi Jia-QiChen JiaBi Yi-YuanWan YangHe YuYang PingLi Min-Hui - Novel therapeutic targets are urgently needed for the aggressive malignancy gallbladder cancer (GBC). G-protein regulated inducer of neurite outgrowth 1 (GPRIN1) is a candidate oncogene, but its function in GBC and its connection to mitochondrial dysregulation remain unknown. In this study, we analyzed clinical samples and demonstrated that GPRIN1 is significantly upregulated in GBC tissues, where its high expression correlates with advanced clinical stage and poor patient prognosis. Functional assays revealed that GPRIN1 is essential for GBC progression, driving cell cycle advancement and maintaining mitochondrial homeostasis. By integrating proteomic and molecular analyses, our study delineates a bimodal and hierarchical regulatory program commanded by GPRIN1 to ensure the robust activation of CDK1. In the nucleus, GPRIN1 functions as a transcriptional co-activator, scaffolding and stabilizing E2F1 to drive CDK1 expression. In parallel, it functions at a post-translational level to directly promote CDK1 activation by physically steering the kinase away from its inhibitor, MYT1, and toward its activator, Cdc25C. This dual-pronged regulation culminates in hyperactivated CDK1, which in turn unleashes a PI3K-Akt signaling cascade to couple relentless cell proliferation with the necessary mitochondrial support. Importantly, genetic or pharmacological disruption of this GPRIN1-CDK1-PI3K/Akt axis completely abrogated tumorigenesis in vitro and in vivo. Taken together, these results reveal GPRIN1 as a master regulator whose dual transcriptional and post-translational control of CDK1 integrates cell cycle progression with mitochondrial homeostasis, suggesting that targeting GPRIN1 may represent a highly specific therapeutic strategy in this lethal malignancy. - Source: PubMed
Publication date: 2026/03/21
Xu ChangGong ZijunNi XiaojianNan LingxiSun WentaoLiu HoubaoLuo XuanmingLi Min - Bisphenols are widely used industrial chemicals with endocrine-disrupting properties, and their potential association with carcinogenesis has drawn considerable attention. Cervical cancer, as a prevalent gynecological malignancy, has a pathogenesis that is not yet fully understood, particularly regarding the influence of environmental factors. In this study, we systematically investigated the molecular effects of bisphenols on cervical cancer using multi-dimensional bioinformatics approaches. WGCNA analysis identified key modules closely associated with the disease, which were integrated with predicted bisphenols targets to screen for core genes, including AR, CDC25C, CDK2, and KIF11. Functional enrichment analysis suggested that bisphenols may disrupt cell cycle regulation, the G2/M checkpoint, and p53-mediated tumor suppressor pathways. Molecular docking and 100-ns molecular dynamics simulations indicated that various bisphenols can stably bind to core target proteins, with binding patterns influenced by halogenation or aromatic substitutions. Gene expression and immunohistochemical analyses showed that CDC25C, CDK2, and KIF11 were significantly upregulated in cervical cancer tissues, whereas AR was predominantly expressed in normal epithelium. Immune infiltration analysis further suggested that CDC25C, CDK2, and KIF11 may modulate the infiltration of B cells, CD8⁺ T cells, and macrophages, implying that bisphenols-induced molecular perturbations could impact the tumor microenvironment. This study provides a reference for further exploration of the links between environmental exposures and cervical cancer development and lays a foundation for mechanistic investigations. - Source: PubMed
Publication date: 2026/02/28
Zi Xue-JiaoLi Yu-LongChu Zi-Yong