ArticleOncotarget2014
MiR-214 and N-ras regulatory loop suppresses rhabdomyosarcoma cell growth and xenograft tumorigenesis.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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.
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Who cites it
28 citing papers in PubMed, 55 citations in OpenAlex.
- Dysregulation of miRNAs in Soft Tissue Sarcomas.Cells · 2024Review
- Rhabdomyosarcoma: Current Therapy, Challenges, and Future Approaches to Treatment Strategies.Cancers · 2023Review
- Genomic and Epigenetic Changes Drive Aberrant Skeletal Muscle Differentiation in Rhabdomyosarcoma.Cancers · 2023Review
- MicroRNAs in the Pathogenesis, Prognostication and Prediction of Treatment Resistance in Soft Tissue Sarcomas.Cancers · 2023Review
- Non-coding RNA in rhabdomyosarcoma progression and metastasis.Frontiers in oncology · 2022Review
- Deletion at an 1q24 locus reveals a critical role of long noncoding RNA DNM3OS in skeletal development.Cell & bioscience · 2021Article
- 6mer Seed Toxicity in Viral microRNAs.iScience · 2020Article
- MicroRNA-29 family inhibits rhabdomyosarcoma formation and progression by regulating GEFT function.American journal of translational research · 2020Article
- miRNA signatures in childhood sarcomas and their clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019Review
- MiRNAs as Players in Rhabdomyosarcoma Development.International journal of molecular sciences · 2019Review
- Co-regulatory Network of Oncosuppressor miRNAs and Transcription Factors for Pathology of Human Hepatic Cancer Stem Cells (HCSC).Scientific reports · 2019Article
- KRAS Oncoprotein Expression Is Regulated by a Self-Governing eIF5A-PEAK1 Feed-Forward Regulatory Loop.Cancer research · 2018Article
- Inhibition of ATG12-mediated autophagy by miR-214 enhances radiosensitivity in colorectal cancer.Oncogenesis · 2018Article
- The role of aberrant expression of T cell miRNAs affected by TNF-α in the immunopathogenesis of rheumatoid arthritis.Arthritis research & therapy · 2017Article
- An Examination of the Role of Transcriptional and Posttranscriptional Regulation in Rhabdomyosarcoma.Stem cells international · 2017Review
- The FOXD3/miR-214/MED19 axis suppresses tumour growth and metastasis in human colorectal cancer.British journal of cancer · 2016Article
- Hedgehog Signaling in Pancreatic Fibrosis and Cancer.Medicine · 2016Review
- miR-214/199a/199a* cluster levels predict poor survival in hepatocellular carcinoma through interference with cell-cycle regulators.Oncotarget · 2016Article
- Small GTPase Arl6 controls RH30 rhabdomyosarcoma cell growth through ciliogenesis and Hedgehog signaling.Cell & bioscience · 2016Article
- MicroRNA dysregulation in rhabdomyosarcoma: a new player enters the game.Cell proliferation · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rhabdomyosarcoma (RMS) is a childhood malignant soft tissue cancer that is derived from myogenic progenitors trapped in a permanent mode of growth. Here, we report that miR-214 is markedly down-regulated in human RMS cell lines. Although not required for embryogenesis in mice, miR-214 suppresses mouse embryonic fibroblast (MEF) proliferation. When re-introduced into RD cells, a line of human embryonal RMS cells, miR-214 showed inhibition of tumor cell growth, induction of myogenic differentiation and apoptosis, as well as suppression of colony formation and xenograft tumorigenesis. We show that in the absence of miR-214, expression of proto-oncogene N-ras is markedly elevated in miR-214(-/-) MEFs, and manipulations of miR-214 levels using microRNA mimics or inhibitor in RD cells reciprocally altered N-ras expression. We further demonstrate that forced expression of N-ras from a cDNA that lacks its 3'-untranslated region neutralized the pro-myogenic and anti-proliferative activities of miR-214. Finally, we show that N-ras is a conserved target of miR-214 in its suppression of xenograft tumor growth, and N-ras expression is up-regulated in xenograft tumor models as well as actual human RMS tissue sections. Taken together, these data indicate that miR-214 is a bona fide suppressor of human RMS tumorigensis.
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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.