ArticleOncotarget2017
MiR-200c is a cMyc-activated miRNA that promotes nasopharyngeal carcinoma by downregulating PTEN.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 42 citations in OpenAlex.
- The paradox of nuclear miRNAs: Mechanisms, therapeutic potential, and future directions.Non-coding RNA research · 2026Review
- Integrated analysis of MYC expression, 8q24.21 copy number, and recurrence patterns in astrocytoma, IDH-mutant.Brain tumor pathology · 2025Article
- Article
- Nuclear-activating miRNAs: unveiling the intricacies of subcellular miRNA function and regulation in cancer and immunity disease.Cancer cell international · 2025Review
- Exploring the tumor-suppressive role of miRNA-200c in head and neck squamous cell carcinoma: Potential and mechanisms of exosome-mediated delivery for therapeutic applications.Translational oncology · 2025Review
- Resveratrol: Targeting Cancer Stem Cells and ncRNAs to Overcome Cancer Drug Resistance.Current molecular medicine · 2024Review
- The Roles of Autophagy-related miRNAs in Gynecologic Tumors: A Review of Current Knowledge for Possible Targeted Therapy.Current molecular medicine · 2024Review
- Review
- MicroRNAs in cancer metastasis: biological and therapeutic implications.Expert reviews in molecular medicine · 2023Review
- MiRNA signatures in nasopharyngeal carcinoma: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2023Review
- The role of miR-200 family in the regulation of hallmarks of cancer.Frontiers in oncology · 2022Review
- The miR-200c/141-ZEB2-TGFβ axis is aberrant in human T-cell prolymphocytic leukemia.Haematologica · 2022Article
- Strategies to Modulate MicroRNA Functions for the Treatment of Cancer or Organ Injury.Pharmacological reviews · 2020Review
- Genetic and expression variations of cell cycle pathway genes in brain tumor patients.Bioscience reports · 2020Article
- Regulatory Mechanism of MicroRNA Expression in Cancer.International journal of molecular sciences · 2020Review
- Suppression of α-methylacyl-coenzyme A racemase by miR200c inhibits prostate adenocarcinoma cell proliferation and migration.Experimental and therapeutic medicine · 2020Article
- Role of Ubiquitination in PTEN Cellular Homeostasis and Its Implications in GB Drug Resistance.Frontiers in oncology · 2020Review
- miR-543 promoted the cell proliferation and invasion of nasopharyngeal carcinoma by targeting the JAM-A.Human cell · 2019Article
- The functions and regulation of the PTEN tumour suppressor: new modes and prospects.Nature reviews. Molecular cell biology · 2018Review
- High miR-718 Suppresses Phosphatase and Tensin Homolog (PTEN) Expression and Correlates to Unfavorable Prognosis in Gastric Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-Myc transcription factor regulates a complex transcriptional program that leads to cellular transformation by targeting a large number of protein-encoding genes and non-coding RNAs. In this study, we show that a microRNA, miR-200c, is a novel c-Myc target that promotes cellular transformation and metastasis in nasopharyngeal carcinoma. MiR-200c achieves this oncogenic effect, at least in part, by targeting and inhibiting the tumor suppressor gene PTEN (phosphatase and tensin homolog), which is a key inhibitor of the AKT kinase signaling that promotes tumorigenesis in nasopharyngeal carcinoma. Our study thus identifies cMyc-miR-200c-PTEN-AKT as a functional module that promotes cellular transformation in nasopharyngeal carcinoma.
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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.