ArticleMolecular cancer research : MCR2016
miR-155 Overexpression Promotes Genomic Instability by Reducing High-fidelity Polymerase Delta Expression and Activating Error-Prone DSB Repair.
Article in Molecular cancer research : MCR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- Molecular landscape and clinical translation of DNA damage response alterations in solid tumors: A pan-cancer perspective on precision oncology.Neoplasia (New York, N.Y.) · 2026Review
- miR-155 aberrant expression impairs tumor rejection because of its targeting of ICOSL and multiple pathways implicated in the antitumor response.Pharmacological reviews · 2026Review
- Polymerase theta inhibition impairs tumor growth and amplifies melphalan-induced DNA damage in multiple myeloma.Journal of translational medicine · 2025Article
- The Dual Role of Dietary Phytochemicals in Oxidative Stress: Implications for Oncogenesis, Cancer Chemoprevention, and ncRNA Regulation.Antioxidants (Basel, Switzerland) · 2025Review
- Beyond proofreading: POLD1 mutations as dynamic orchestrators of genomic instability and immune evasion in cancer.Frontiers in immunology · 2025Review
- ECM Proteins Nidogen-1 and Decorin Restore Functionality of Human Islets of Langerhans upon Hypoxic Conditions.Advanced healthcare materials · 2025Article
- MicroRNAs as key regulators of cancer drug resistance: insights and future directions in chemotherapy, targeted-therapy, radiotherapy, and immunotherapy.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Article
- The association between inefficient repair of oxidative DNA lesions and common polymorphisms of the key base excision repair genes as well as their expression levels in patients with rheumatoid arthritis.Archives of medical science : AMS · 2025Article
- A cross-sectional study comparing the expression of DNA repair molecules in subjects with and without atherosclerotic plaques.Molecular biology reports · 2024Article
- Prospects of POLD1 in Human Cancers: A Review.Cancers · 2023Review
- Differential miRNA expression of hypoxic MCF7 and PANC-1 cells.Frontiers in endocrinology · 2023Article
- Exploiting DNA Ligase III addiction of multiple myeloma by flavonoid Rhamnetin.Journal of translational medicine · 2022Article
- Response to neoadjuvant chemotherapy in breast cancer: do microRNAs matter?Discover oncology · 2022Article
- Interrelationship between miRNA and splicing factors in pancreatic ductal adenocarcinoma.Epigenetics · 2022Review
- Interactions between miRNAs and Double-Strand Breaks DNA Repair Genes, Pursuing a Fine-Tuning of Repair.International journal of molecular sciences · 2022Review
- Article
- Roles of miRNA dysregulation in the pathogenesis of multiple myeloma.Cancer gene therapy · 2021Review
- Therapeutic targeting of the hypoxic tumour microenvironment.Nature reviews. Clinical oncology · 2021Review
- MEK1/2 regulates APOBEC3B and polymerase iota-induced mutagenesis in head and neck cancer cells.American journal of cancer research · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledmiR-155 is an oncogenic miRNA that is often overexpressed in cancer and is associated with poor prognosis. miR-155 can target several DNA repair factors, including RAD51, MLH1, and MSH6, and its overexpression results in an increased mutation frequency in vitro, although the mechanism has yet to be fully understood. Here, we demonstrate that overexpression of miR-155 drives an increased mutation frequency both in vitro and in vivo, promoting genomic instability by affecting multiple DNA repair pathways. miR-155 overexpression causes a decrease in homologous recombination, but yields a concurrent increase in the error-prone nonhomologous end-joining pathway. Despite repressing established targets MLH1 and MSH6, the identified mutation pattern upon miR-155 overexpression does not resemble that of a mismatch repair-deficient background. Further investigation revealed that all four subunits of polymerase delta, a high-fidelity DNA replication, and repair polymerase are downregulated at the mRNA level in the context of miR-155 overexpression. FOXO3a, a transcription factor and known target of miR-155, has one or more putative binding site(s) in the promoter of all four polymerase delta subunits. Finally, suppression of FOXO3a by miR-155 or by siRNA knockdown is sufficient to repress the expression of the catalytic subunit of polymerase delta, POLD1, at the protein level, indicating that FOXO3a contributes to the regulation of polymerase delta levels. IMPLICATIONS: Taken together, miR-155 overexpression drives an increase in mutation frequency via multifaceted impact on DNA damage response and DNA repair pathways.
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