ArticleCancer science2021
MCM10 compensates for Myc-induced DNA replication stress in breast cancer stem-like cells.
Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Pooled it
- MCM10, a novel YAP1/TEAD4 target, drives gastric cancer progression by bridging DNA replication to stemness acquisition.Molecular cancer · 2026Article
- High MCM10 expression mediates TMZ resistance and promotes the progression of glioma.Cancer chemotherapy and pharmacology · 2025Article
- Overexpression of MCM3 as a prognostic biomarker correlated with cell proliferation, cell cycle and immune regulation in hepatocellular carcinoma.Journal of Cancer · 2025Article
- GAIN-BRCA: a graph-based AI-net framework for breast cancer subtype classification using multiomics data.Bioinformatics advances · 2025Article
- Multifaceted role of the DNA replication protein MCM10 in maintaining genome stability and its implication in human diseases.Cancer metastasis reviews · 2024Review
- Review
- Single-molecule characterization of SV40 replisome and novel factors: human FPC and Mcm10.Nucleic acids research · 2024Article
- Replication Stress in Activated Human NK Cells Induces Sensitivity to Apoptosis.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Targeting DHX9 Triggers Tumor-Intrinsic Interferon Response and Replication Stress in Small Cell Lung Cancer.Cancer discovery · 2024Article
- Dormant cancer cells and polyploid giant cancer cells: The roots of cancer recurrence and metastasis.Clinical and translational medicine · 2024Review
- Identification of cancer stem cell-related genes through single cells and machine learning for predicting prostate cancer prognosis and immunotherapy.Frontiers in immunology · 2024Article
- Activation of Glycolysis by MCM10 Increases Stemness and Paclitaxel Resistance in Gastric Cancer Cells.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023Article
- MCM10, a potential diagnostic, immunological, and prognostic biomarker in pan-cancer.Scientific reports · 2023Article
- Review
- Protooncogenic Role ofBioMed research international · 2023Article
- Immune modulation and prognostic significance of MCM10 in pan-cancer: a comprehensive analysis.American journal of translational research · 2023Article
- Application of Protein-Protein Interaction Network Analysis in Order to Identify Cervical Cancer miRNA and mRNA Biomarkers.TheScientificWorldJournal · 2023Article
- MCM10 expression is linked to cervical cancer aggressiveness.Frontiers in molecular medicine · 2023Article
- Identification of Novel Hub Genes Associated with Psoriasis Using Integrated Bioinformatics Analysis.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
27 authors at 9 institutions in 3 countries.
Funding
Abstract
Cancer stem-like cells (CSCs) induce drug resistance and recurrence of tumors when they experience DNA replication stress. However, the mechanisms underlying DNA replication stress in CSCs and its compensation remain unclear. Here, we demonstrate that upregulated c-Myc expression induces stronger DNA replication stress in patient-derived breast CSCs than in differentiated cancer cells. Our results suggest critical roles for mini-chromosome maintenance protein 10 (MCM10), a firing (activating) factor of DNA replication origins, to compensate for DNA replication stress in CSCs. MCM10 expression is upregulated in CSCs and is maintained by c-Myc. c-Myc-dependent collisions between RNA transcription and DNA replication machinery may occur in nuclei, thereby causing DNA replication stress. MCM10 may activate dormant replication origins close to these collisions to ensure the progression of replication. Moreover, patient-derived breast CSCs were found to be dependent on MCM10 for their maintenance, even after enrichment for CSCs that were resistant to paclitaxel, the standard chemotherapeutic agent. Further, MCM10 depletion decreased the growth of cancer cells, but not of normal cells. Therefore, MCM10 may robustly compensate for DNA replication stress and facilitate genome duplication in cancer cells in the S-phase, which is more pronounced in CSCs. Overall, we provide a preclinical rationale to target the c-Myc-MCM10 axis for preventing drug resistance and recurrence of tumors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.