ArticleProceedings of the National Academy of Sciences of the United States of America2010
Modulation of mismatch repair and genomic stability by miR-155.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
181 citing papers in PubMed, 1 synthesis or guideline pooled it, 349 citations in OpenAlex.
- Pooled it
- Review
- The harmonies played by miR-302/367 cluster in pluripotency, reprogramming, and rejuvenation.Stem cells translational medicine · 2026Review
- Targeted Inhibition of Oncogenic microRNAs miR-21, miR-17, and miR-155 Suppresses Tumor Growth and Modulates Immune Response in Colorectal Cancer.Pharmaceutics · 2026Article
- New Insights from the Expression of the Mismatch Repair System in Pituitary Neuroendocrine Tumors.Endocrine pathology · 2026Article
- miR-155 aberrant expression impairs tumor rejection because of its targeting of ICOSL and multiple pathways implicated in the antitumor response.Pharmacological reviews · 2026Review
- Mismatch Repair as a Dynamic and Clinically Actionable Vulnerability in Cancer.Cancer research · 2025Review
- SOX10, MITF, and microRNAs: Decoding their interplay in regulating melanoma plasticity.International journal of cancer · 2025Review
- Pharmacological interventions targeting β-adrenoceptors in colorectal cancer: an evolving paradigm.Inflammopharmacology · 2025Review
- Review
- Review
- MiR5651, miR170-3p, and miR171a-3p Regulate Cadmium Tolerance by TargetingPlants (Basel, Switzerland) · 2025Article
- Molecular insights into immune evasion and therapeutic paradigms in pancreatic cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- Dual role of miR-155 and exosomal miR-155 in tumor angiogenesis: implications for cancer progression and therapy.European journal of medical research · 2025Review
- Clinical significance of long non-coding RNA MIR155HG genetic variants and susceptibility to oral cancer.Scientific reports · 2025Article
- Ionizing Radiation May Induce Tumors Partly Through the Alteration or Regulation of Mismatch Repair Genes.Cancers · 2025Review
- Carcinogenesis trajectories.Frontiers in cell and developmental biology · 2025Article
- Circadian genes and non-coding RNAs: interactions and implications in cancer.Animal cells and systems · 2025Review
- A cross-sectional study comparing the expression of DNA repair molecules in subjects with and without atherosclerotic plaques.Molecular biology reports · 2024Article
- Overlooked poor-quality patient samples in sequencing data impair reproducibility of published clinically relevant datasets.Genome biology · 2024Article
121 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 4 institutions in 2 countries.
Funding
Abstract
Inactivation of mismatch repair (MMR) is the cause of the common cancer predisposition disorder Lynch syndrome (LS), also known as hereditary nonpolyposis colorectal cancer (HNPCC), as well as 10-40% of sporadic colorectal, endometrial, ovarian, gastric, and urothelial cancers. Elevated mutation rates (mutator phenotype), including simple repeat instability [microsatellite instability (MSI)] are a signature of MMR defects. MicroRNAs (miRs) have been implicated in the control of critical cellular pathways involved in development and cancer. Here we show that overexpression of miR-155 significantly down-regulates the core MMR proteins, hMSH2, hMSH6, and hMLH1, inducing a mutator phenotype and MSI. An inverse correlation between the expression of miR-155 and the expression of MLH1 or MSH2 proteins was found in human colorectal cancer. Finally, a number of MSI tumors with unknown cause of MMR inactivation displayed miR-155 overexpression. These data provide support for miR-155 modulation of MMR as a mechanism of cancer pathogenesis.
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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.