ArticleOncogene2010
Minichromosome maintenance proteins 2, 3 and 7 in medulloblastoma: overexpression and involvement in regulation of cell migration and invasion.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 89 citations in OpenAlex.
- Mechanism of Anticancer Activity of Cedrol in Epidermal Carcinoma Cells and Its Validation in 3D Artificial Skin Model.Journal of microbiology and biotechnology · 2026Article
- Heterogeneous Expression Patterns of the Minichromosome Maintenance Complex Members in Retinoblastoma Unveil Its Clinical Significance.Investigative ophthalmology & visual science · 2024Article
- The prognostic and immunological role of MCM3 in pan-cancer and validation of prognosis in a clinical lower-grade glioma cohort.Frontiers in pharmacology · 2024Article
- MCM4 acts as a biomarker for LUAD prognosis.Journal of cellular and molecular medicine · 2023Article
- Identification of tumor antigens and immune subtypes of hepatocellular carcinoma for mRNA vaccine development.World journal of gastrointestinal oncology · 2023Article
- Risk model based on minichromosome maintenance 2 using objective assessment for predicting survival of neuroblastoma.iScience · 2023Article
- O-GlcNAcylation of YTHDF2 promotes HBV-related hepatocellular carcinoma progression in an NSignal transduction and targeted therapy · 2023Article
- Cedrol, a Sesquiterpene Isolated from Juniperus chinensis, Inhibits Human Colorectal Tumor Growth associated through Downregulation of Minichromosome Maintenance Proteins.Journal of cancer prevention · 2022Article
- MCM2 in human cancer: functions, mechanisms, and clinical significance.Molecular medicine (Cambridge, Mass.) · 2022Review
- Induction of Cell Cycle Arrest, Apoptosis, and Reducing the Expression of MCM Proteins in Human Lung Carcinoma A549 Cells by Cedrol, Isolated fromJournal of microbiology and biotechnology · 2022Article
- ITRAQ-based quantitative proteomic analysis reveals that VPS35 promotes the expression of MCM2-7 genes in HeLa cells.Scientific reports · 2022Article
- The Deubiquitinase USP39 Promotes Esophageal Squamous Cell Carcinoma Malignancy as a Splicing Factor.Genes · 2022Article
- A DNA replication-independent function of pre-replication complex genes during cell invasion in C. elegans.PLoS biology · 2022Article
- Eukaryotic translation initiation factor 3 subunit B could serve as a potential prognostic predictor for breast cancer.Bioengineered · 2022Article
- Prereplication complex proteins get caught moonlighting.PLoS biology · 2022Article
- Bioinformatics approaches identified dasatinib and bortezomib inhibit the activity of MCM7 protein as a potential treatment against human cancer.Scientific reports · 2022Article
- Radiation Necrosis with Proton Therapy in a Patient with Aarskog-Scott Syndrome and Medulloblastoma.International journal of particle therapy · 2022Article
- High content genome-wide siRNA screen to investigate the coordination of cell size and RNA production.Scientific data · 2021Article
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2 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Minichromosome maintenance (MCM) proteins 2-7 are important in DNA replication licensing. Functional roles beyond licensing are speculated. In addition, significances in medulloblastoma (MB) remain unclear. In this study, we showed the frequent deregulation of MCM2 and MCM3 expression in 7 MB cell lines and 31 clinical samples. Moreover, DAOY and ONS76 and the clinical samples expressed elevated MCM7 transcripts with genomic gain of the gene. Immunopositivity restricted to tumor cells was found in 41, 37 and 53 out of 73 MB cases for MCM2, MCM3 and MCM7, respectively. High-MCM3 expression was associated with poor prognosis. Knockdowns of these MCMs significantly inhibited anchorage-dependent and -independent MB cell growth. The inhibition of MCM3 expression by small interfering RNA knockdown was related to G1 arrest with reduced cyclin A expression, whereas the MCM2- and MCM7-knocked-down cells arrested at G2/M with increased cyclin A expression. Interestingly, we demonstrated the links of these MCMs with cell migration and invasion using wound-healing and Transwell migration/invasion assays. Exogenous overexpression of MCM2, MCM3 and MCM7 increased anchorage-independent cell growth, and also cell migration and invasion capabilities in MB cells. The knockdown reduced the number of filopodial cells and the cells with intense stress fibers by blocking cdc42 and Rho activation. Taken together, deregulation of MCM2, MCM3 and MCM7 expression might be involved in MB tumorigenesis and we revealed undefined roles of these MCMs in control of MB cell migration and invasion.
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