ArticleThe Journal of pathology2015
Constitutive ERK1/2 activation contributes to production of double minute chromosomes in tumour cells.
Article in The Journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Initial Screening of Extrachromosomal Circular DNA Candidates for Pork Meat Quality Traits Using Circle-Seq and RNA-Seq Analysis.Animals : an open access journal from MDPI · 2025Article
- Repression of the SUMO-conjugating enzyme UBC9 is associated with lowered double minutes and reduced tumor progression.Cancer biology & therapy · 2024Article
- Unveiling the mysteries of extrachromosomal circular DNA: from generation to clinical relevance in human cancers and health.Molecular cancer · 2024Review
- Reduced chemokine C-C motif ligand 1 expression may negatively regulate colorectal cancer progression at liver metastatic sites.Journal of cellular and molecular medicine · 2024Article
- Innovative insights into extrachromosomal circular DNAs in gynecologic tumors and reproduction.Protein & cell · 2024Review
- Circle-seq reveals that eccDNA may be a key blood biomarker for HBV-associated liver cancer.Frontiers in genetics · 2024Article
- Extrachromosomal circular DNA: biogenesis, structure, functions and diseases.Signal transduction and targeted therapy · 2022Review
- Plasticity of Extrachromosomal and Intrachromosomal BRAF Amplifications in Overcoming Targeted Therapy Dosage Challenges.Cancer discovery · 2022Article
- [Amplification of Extrachromosomal Oncogene and Tumorigenesis and Development].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2020Review
- Novel insights into extrachromosomal DNA: redefining the onco-drivers of tumor progression.Journal of experimental & clinical cancer research : CR · 2020Review
- Sei-1 promotes double minute chromosomes formation through activation of the PI3K/Akt/BRCA1-Abraxas pathway and induces double-strand breaks in NIH-3T3 fibroblasts.Cell death & disease · 2018Article
- EWS-FLI1 and RNA helicase A interaction inhibitor YK-4-279 inhibits growth of neuroblastoma.Oncotarget · 2017Article
- TRIB1 promotes colorectal cancer cell migration and invasion through activation MMP-2 via FAK/Src and ERK pathways.Oncotarget · 2017Article
- Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways.Scientific reports · 2017Article
- Met promotes the formation of double minute chromosomes induced by Sei-1 in NIH-3T3 murine fibroblasts.Oncotarget · 2016Article
- MAPK1/ERK2 as novel target genes for pain in head and neck cancer patients.BMC genetics · 2016Article
- Gene-based analysis of the fibroblast growth factor receptor signaling pathway in relation to breast cancer in African American women: the AMBER consortium.Breast cancer research and treatment · 2016Article
Corrections and comments
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Authors and funding
24 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Double minute chromosomes (DMs) are extrachromosomal cytogenetic structures found in tumour cells. As hallmarks of gene amplification, DMs often carry oncogenes and drug-resistance genes and play important roles in malignant tumour progression and drug resistance. The mitogen-activated protein kinase (MAPK) signalling pathway is frequently dysregulated in human malignant tumours, which induces genomic instability, but it remains unclear whether a close relationship exists between MAPK signalling and DMs. In the present study, we focused on three major components of MAPK signalling, ERK1/2, JNK1/2/3 and p38, to investigate the relationship between MAPK and DM production in tumour cells. We found that the constitutive phosphorylation of ERK1/2, but not JNK1/2/3 and p38, was closely associated with DMs in tumour cells. Inhibition of ERK1/2 activation in DM-containing and ERK1/2 constitutively phosphorylated tumour cells was able to markedly decrease the number of DMs, as well as the degree of amplification and expression of DM-carried genes. The mechanism was found to be an increasing tendency of DM DNA to break, become enveloped into micronuclei (MNs) and excluded from the tumour cells during the S/G2 phases of the cell cycle, events that accompanied the reversion of malignant behaviour. Our study reveals a linkage between ERK1/2 activation and DM stability in tumour cells.
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