ArticleInternational journal of cancer2019
Inhibiting homologous recombination decreases extrachromosomal amplification but has no effect on intrachromosomal amplification in methotrexate-resistant colon cancer cells.
Article in International journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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.
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Who cites it
39 citing papers in PubMed, 64 citations in OpenAlex.
- EZH2 deficiency suppresses colorectal cancer progression by inhibiting the mismatch repair pathway and consequently reducing extrachromosomal circular DNA formation.Cell death & disease · 2026Article
- The potential clinical implications of extrachromosomal circular DNA as a biomarker.Genes & diseases · 2026Review
- Targeting extrachromosomal DNA in human cancers.Nature reviews. Drug discovery · 2026Review
- Dysfunctional DNA Mismatch Repair Drives the Evolution of Gene Amplification in MTX-Resistant Human Colorectal Cancer Cells.International journal of molecular sciences · 2026Article
- Extrachromosomal circular DNA: a potential clinical therapeutic target in malignant tumors.Cellular & molecular biology letters · 2026Review
- Extrachromosomal DNA and cancer: function, formation, and clinical implications.Journal of experimental & clinical cancer research : CR · 2026Review
- DNA repair pathway-related proteins are involved in the circularization step of microDNA eccDNACommunications biology · 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
- Dynamic genomic changes in methotrexate-resistant human cancer cell lines beyond DHFR amplification suggest potential new targets for preventing drug resistance.British journal of cancer · 2024Article
- Review
- Circle-seq reveals that eccDNA may be a key blood biomarker for HBV-associated liver cancer.Frontiers in genetics · 2024Article
- Novel insights into the ecDNA formation mechanism involving MSH3 in methotrexate‑resistant human colorectal cancer cells.International journal of oncology · 2023Article
- Small extrachromosomal circular DNA harboring targeted tumor suppressor gene mutations supports intratumor heterogeneity in mouse liver cancer induced by multiplexed CRISPR/Cas9.Genome medicine · 2023Article
- Gene amplifications and extrachromosomal circular DNAs: function and biogenesis.Molecular biology reports · 2023Review
- The characteristics of extrachromosomal circular DNA in patients with end-stage renal disease.European journal of medical research · 2023Article
- Extrachromosomal circular DNA in colorectal cancer: biogenesis, function and potential as therapeutic target.Oncogene · 2023Review
- Extrachromosomal circular DNA: biogenesis, structure, functions and diseases.Signal transduction and targeted therapy · 2022Review
- Life of double minutes: generation, maintenance, and elimination.Chromosoma · 2022Review
- Extrachromosomal circular DNA (eccDNA): an emerging star in cancer.Biomarker research · 2022Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gene amplification, which involves the two major topographical structures double minutes (DMs) and homegeneously stained region (HSR), is a common mechanism of treatment resistance in cancer and is initiated by DNA double-strand breaks. NHEJ, one of DSB repair pathways, is involved in gene amplification as we demonstrated previously. However, the involvement of homologous recombination, another DSB repair pathway, in gene amplification remains to be explored. To better understand the association between HR and gene amplification, we detected HR activity in DM- and HSR-containing MTX-resistant HT-29 colon cancer cells. In DM-containing MTX-resistant cells, we found increased homologous recombination activity compared with that in MTX-sensitive cells. Therefore, we suppressed HR activity by silencing BRCA1, the key player in the HR pathway. The attenuation of HR activity decreased the numbers of DMs and DM-form amplified gene copies and increased the exclusion of micronuclei and nuclear buds that contained DM-form amplification; these changes were accompanied by cell cycle acceleration and increased MTX sensitivity. In contrast, BRCA1 silencing did not influence the number of amplified genes and MTX sensitivity in HSR-containing MTX-resistant cells. In conclusion, our results suggest that the HR pathway plays different roles in extrachromosomal and intrachromosomal gene amplification and may be a new target to improve chemotherapeutic outcome by decreasing extrachromosomal amplification in cancer.
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