ReviewOncogene2023
The CMG helicase and cancer: a tumor "engine" and weakness with missing mutations.
Review in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- MCM5 UFMylation regulates replication origin firing and fork progression.The EMBO journal · 2025Article
- TRIM21 promotes colorectal cancer development through regulating DNA replication by TCF3/MCM2/5 axis.Cell death discovery · 2025Article
- DDX27 in cancer: molecular mechanisms, clinical implications, and therapeutic potential.Journal of translational medicine · 2025Review
- Oncogenic Activity and Sorafenib Sensitivity ofCancers · 2025Article
- USP37 prevents unscheduled replisome unloading through MCM complex deubiquitination.Nature communications · 2025Article
- Critical and differential roles of eIF4A1 and eIF4A2 in B-cell development and function.Cellular & molecular immunology · 2025Article
- Recent advances in therapeutic use of transforming growth factor-beta inhibitors in cancer and fibrosis.Frontiers in oncology · 2025Review
- Multifaceted role of the DNA replication protein MCM10 in maintaining genome stability and its implication in human diseases.Cancer metastasis reviews · 2024Review
- Identification of ATP-Competitive Human CMG Helicase Inhibitors for Cancer Intervention that Disrupt CMG-Replisome Function.Molecular cancer therapeutics · 2024Article
- [Relationship between GTSE1 and Cell Cycle and Potential Regulatory Mechanisms in Lung Cancer Cells].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Review
- Induction of the humanMolecular medicine reports · 2024Article
- Unwinding Helicase MCM Functionality for Diagnosis and Therapeutics of Replication Abnormalities Associated with Cancer: A Review.Molecular diagnosis & therapy · 2024Review
- Combined therapy of dabrafenib and an anti-HER2 antibody-drug conjugate for advanced BRAF-mutant melanoma.Cellular & molecular biology letters · 2024Article
- GINS2 regulates temozolomide chemosensitivity via the EGR1/ECT2 axis in gliomas.Cell death & disease · 2024Article
- MCM5 is a Novel Therapeutic Target for Glioblastoma.OncoTargets and therapy · 2024Article
- Modeling phenotypic heterogeneity towards evolutionarily inspired osteosarcoma therapy.Scientific reports · 2023Article
- FOXP1-GINS1 axis promotes DLBCL proliferation and directs doxorubicin resistance.Journal of Cancer · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The replicative Cdc45-MCM-GINS (CMG) helicase is a large protein complex that functions in the DNA melting and unwinding steps as a component of replisomes during DNA replication in mammalian cells. Although the CMG performs this important role in cell growth, the CMG is not a simple bystander in cell cycle events. Components of the CMG, specifically the MCM precursors, are also involved in maintaining genomic stability by regulating DNA replication fork speeds, facilitating recovery from replicative stresses, and preventing consequential DNA damage. Given these important functions, MCM/CMG complexes are highly regulated by growth factors such as TGF-ß1 and by signaling factors such as Myc, Cyclin E, and the retinoblastoma protein. Mismanagement of MCM/CMG complexes when these signaling mediators are deregulated, and in the absence of the tumor suppressor protein p53, leads to increased genomic instability and is a contributor to tumorigenic transformation and tumor heterogeneity. The goal of this review is to provide insight into the mechanisms and dynamics by which the CMG is regulated during its assembly and activation in mammalian genomes, and how errors in CMG regulation due to oncogenic changes promote tumorigenesis. Finally, and most importantly, we highlight the emerging understanding of the CMG helicase as an exploitable vulnerability and novel target for therapeutic intervention in cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.