ArticleInternational journal of radiation oncology, biology, physics2014
microRNA alterations driving acute and late stages of radiation-induced fibrosis in a murine skin model.
Article in International journal of radiation oncology, biology, physics, 2014. 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, 24 citations in OpenAlex.
- LiposomalInternational journal of molecular sciences · 2026Article
- Presymptomatic microRNA-based biomarker signatures for the prognosis of localized radiation injury in mice.PloS one · 2025Article
- microRNA blood signature for localized radiation injury.Scientific reports · 2024Article
- Radiation-induced circulating microRNAs linked to echocardiography parameters after radiotherapy.Frontiers in oncology · 2023Article
- MicroRNA-34a: A Novel Therapeutic Target in Fibrosis.Frontiers in physiology · 2022Review
- Exosome-mediated radiosensitizing effect on neighboring cancer cells via increase in intracellular levels of reactive oxygen species.Oncology reports · 2021Article
- MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers.Frontiers in cell and developmental biology · 2020Review
- Article
- Reactive Oxygen Species Drive Epigenetic Changes in Radiation-Induced Fibrosis.Oxidative medicine and cellular longevity · 2019Review
- Regulation of Cellular Senescence by miR-34a in Alcoholic Liver Injury.The American journal of pathology · 2017Article
- Radiation-Induced Fibrosis: Mechanisms and Opportunities to Mitigate. Report of an NCI Workshop, September 19, 2016.Radiation research · 2017Article
- MicroRNA expression signature and the therapeutic effect of the microRNA‑21 antagomir in hypertrophic scarring.Molecular medicine reports · 2017Article
- Emergence of miR-34a in radiation therapy.Critical reviews in oncology/hematology · 2017Review
- Loss of miR-140 is a key risk factor for radiation-induced lung fibrosis through reprogramming fibroblasts and macrophages.Scientific reports · 2016Article
- Radiogenomics: A systems biology approach to understanding genetic risk factors for radiotherapy toxicity?Cancer letters · 2016Review
- The Anti-fibrotic Effects and Mechanisms of MicroRNA-486-5p in Pulmonary Fibrosis.Scientific reports · 2015Article
- MicroRNA in radiotherapy: miRage or miRador?British journal of cancer · 2015Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
purposeAlthough ionizing radiation is critical in treating cancer, radiation-induced fibrosis (RIF) can have a devastating impact on patients' quality of life. The molecular changes leading to radiation-induced fibrosis must be elucidated so that novel treatments can be designed. METHODS AND MATERIALS: To determine whether microRNAs (miRs) could be responsible for RIF, the fibrotic process was induced in the right hind legs of 9-week old CH3 mice by a single-fraction dose of irradiation to 35 Gy, and the left leg served as an unirradiated control. Fibrosis was quantified by measurements of leg length compared with control leg length. By 120 days after irradiation, the irradiated legs were 20% (P=.013) shorter on average than were the control legs.
resultsTissue analysis was done on muscle, skin, and subcutaneous tissue from irradiated and control legs. Fibrosis was noted on both gross and histologic examination by use of a pentachrome stain. Microarrays were performed at various times after irradiation, including 7 days, 14 days, 50 days, 90 days, and 120 days after irradiation. miR-15a, miR-21, miR-30a, and miR-34a were the miRs with the most significant alteration by array with miR-34a, proving most significant on confirmation by reverse transcriptase polymerase chain reaction, c-Met, a known effector of fibrosis and downstream molecule of miR-34a, was evaluated by use of 2 cell lines: HCT116 and 1522. The cell lines were exposed to various stressors to induce miR changes, specifically ionizing radiation. Additionally, in vitro transfections with pre-miRs and anti-miRs confirmed the relationship of miR-34a and c-Met.
conclusionsOur data demonstrate an inverse relationship with miR-34a and c-Met; the upregulation of miR-34a in RIF causes inhibition of c-Met production. miRs may play a role in RIF; in particular, miR-34a should be investigated as a potential target to prevent or treat this devastating side effect of irradiation.
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Registered trials
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