ArticleFrontiers in oncology2023
CEP55 as a promising biomarker and therapeutic target on gallbladder cancer.
Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Prognostic significance of CEP55 expression in non-small cell lung cancer: a systematic review and meta-analysis.BMC pulmonary medicine · 2026Pooled it
- WTAP-mediated mMolecular genetics and genomics : MGG · 2026Article
- CEP55 promotes prostate cancer progression via TPX2-dependent activation of AURKA-PI3K-AKT signaling and inhibition of ferroptosis.The Journal of biological chemistry · 2026Article
- Integrating bulk RNA-seq and ScRNA-seq to identify manganese metabolism-related subtypes and immunoregulatory mechanisms in liver hepatocellular carcinoma.Open life sciences · 2026Article
- Mechanisms of Ferroptosis-Related Genes in Gallbladder Cancer Based on Bioinformatics Analysis.Molecular biotechnology · 2025Article
- Clinical potential and experimental validation of prognostic genes in hepatocellular carcinoma revealed by risk modeling utilizing single cell and transcriptome constructs.Frontiers in immunology · 2025Article
- ALKBH5 activates CEP55 transcription through m6A demethylation in FOXP2 mRNA and expedites cell cycle entry and EMT in ovarian cancer.Biology direct · 2024Article
- TGF-β1 facilitates gallbladder carcinoma metastasis by regulating FOXA1 translation efficiency through mCell death & disease · 2024Article
- Knockdown of TOP2A suppresses IL-17 signaling pathway and alleviates the progression of ulcerative colitis.Immunity, inflammation and disease · 2024Article
- New trends in diagnosis and management of gallbladder carcinoma.World journal of gastrointestinal oncology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Gallbladder cancer (GBC) is a highly malignant biliary tumor with a poor prognosis. As existing therapies for advanced metastatic GBC are rarely effective, there is an urgent need to identify more effective targets for treatment. Methods: Hub genes of GBC were identified by bioinformatics analysis and their expression in GBC was analyzed by tissue validation. The biological role of CEP55 in GBC cell and the underlying mechanism of the anticancer effect of CEP55 knockdown were evaluated via CCK8, colony formation assay, EDU staining, flow cytometry, western blot, immunofluorescence, and an alkaline comet assay. Results: We screened out five hub genes of GBC, namely PLK1, CEP55, FANCI, NEK2 and PTTG1. CEP55 is not only overexpressed in the GBC but also correlated with advanced TNM stage, differentiation grade and poorer survival. After CEP55 knockdown, the proliferation of GBC cells was inhibited with cell cycle arrest in G2/M phase and DNA damage. There was a marked increase in the apoptosis of GBC cells in the siCEP55 group. Besides, in vivo, CEP55 inhibition attenuated the growth and promoted apoptosis of GBC cells. Mechanically, the tumor suppressor effect of CEP55 knockdown is associated with dysregulation of the AKT and ERK signaling networks. Discussion: These data not only demonstrate that CEP55 is identified as a potential independent predictor crucial to the diagnosis and prognosis of gallbladder cancer but also reveal the possibility for CEP55 to be used as a promising target in the treatment of GBC.
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