ArticleOncogene2021
MCM8 is regulated by EGFR signaling and promotes the growth of glioma stem cells through its interaction with DNA-replication-initiating factors.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Structural Activation of DNA Unwinding by MCM8/9/HROB.bioRxiv : the preprint server for biology · 2026Article
- SDF2L1 modulates oxLDL-induced endoplasmic reticulum stress, protein aggregation, and O-mannosylation in myocardial infarction and lung cancer.Cellular and molecular life sciences : CMLS · 2026Article
- MCM8 promotes colorectal cancer progression by competitively inhibiting HRD1-mediated CDC42 ubiquitination and degradation.Journal of translational medicine · 2026Article
- Single-cell analysis identifies a VIM+ glioma stem-like vascular-immune state linked to myeloid OSM signaling and CEBPD activity.Frontiers in immunology · 2026Article
- Identification and validation of biomarkers related to mismatch repair for prognosis prediction in glioma.Frontiers in immunology · 2026Article
- RBM15 is a novel prognostic biomarker and correlates with immune cell infiltration in lung adenocarcinoma.Journal of cardiothoracic surgery · 2025Article
- AmNA-Modified Antisense Oligonucleotide Targeting MCM8 as a Cancer-Specific Chemosensitizer for Platinum Compounds.Cancer science · 2025Article
- CCL2 mediated IKZF1 expression promotes M2 polarization of glioma-associated macrophages through CD84-SHP2 pathway.Oncogene · 2024Article
- MCM8 promotes lung cancer progression through upregulating DNAJC10.Journal of cellular and molecular medicine · 2024Article
- A Mettl16/mThe EMBO journal · 2024Article
- Mechanism of DNA unwinding by MCM8-9 in complex with HROB.Nature communications · 2024Article
- Expressions of the satellite repeat HSAT5 and transposable elements are implicated in disease progression and survival in glioma.Turkish journal of biology = Turk biyoloji dergisi · 2024Article
- Function and mechanism of MCM8 in the development and progression of colorectal cancer.Journal of translational medicine · 2023Article
- Mechanism of DNA unwinding by hexameric MCM8-9 in complex with HROB.Research square · 2023Article
- Enhancer-driven transcription of MCM8 by E2F4 promotes ATR pathway activation and glioma stem cell characteristics.Hereditas · 2023Article
- The Recent Research Progress of NF-κB Signaling on the Proliferation, Migration, Invasion, Immune Escape and Drug Resistance of Glioblastoma.International journal of molecular sciences · 2023Review
- Review
- The U2AF65/circNCAPG/RREB1 feedback loop promotes malignant phenotypes of glioma stem cells through activating the TGF-β pathway.Cell death & disease · 2023Article
- Immune modulation and prognostic significance of MCM10 in pan-cancer: a comprehensive analysis.American journal of translational research · 2023Article
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mini-chromosome maintenance (MCM) proteins are critical components of DNA-replication-licensing factors. MCM8 is an MCM protein that exhibits oncogenic functions in several human malignancies. However, the role of MCM8 in glioblastomas (GBMs) has remained unclear. In the present study, we investigated the biological functions and mechanisms of MCM8 in glioma stem cells (GSCs). The clinical relevance of MCM8 mRNA expression was explored via TCGA and REMBRANDT datasets. The effects of MCM8 on the self-renewal and tumorigenicity of GSCs were examined both in vitro and in vivo. The regulation of MCM8 expression and its interacting proteins were also evaluated. We found that the expression of MCM8 was elevated in high-grade gliomas and classical molecular subtypes and was inversely correlated with patient prognosis. GSCs had a significantly higher expression of MCM8 compared with that in normal glioma cells. Silencing of MCM8 induced G0/G1 arrest and apoptosis, as well as inhibited the proliferation and self-renewal of GSCs. Forced expression of MCM8 enhanced clonogenicity of GSCs both in vitro and in vivo. MCM8 expression was regulated by EGFR signaling, which was mediated by NF-κB (p65). MCM8 interacted with DNA-replication-initiating factors-including EZH2, CDC6, and CDCA2-and influenced these factors to associate with chromatin. In addition, MCM8 knockdown increased the sensitivity of GSCs to radiation and TMZ treatments. Our findings suggest that MCM8, regulated by the EGFR pathway, maintains the clonogenic and tumorigenic potential of GSCs through interaction with DNA-replication-initiating factors; hence, MCM8 may represent a novel therapeutic target in GBMs.
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