ArticleProceedings of the National Academy of Sciences of the United States of America2011
MicroRNA-149*, a p53-responsive microRNA, functions as an oncogenic regulator in human melanoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 3 of them syntheses 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.
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Who cites it
100 citing papers in PubMed, 3 syntheses or guidelines pooled it, 180 citations in OpenAlex.
- MicroRNAs as potential signatures of environmental exposure or effect: a systematic review.Environmental health perspectives · 2015Pooled it
- Effects of four single nucleotide polymorphisms in microRNA-coding genes on lung cancer risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- The association between two microRNA variants (miR-499, miR-149) and gastrointestinal cancer risk: a meta-analysis.PloS one · 2013Pooled it
- Review
- Non-coding RNAs in BRAF-mutant melanoma: targets, indicators, and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- A Critical Review on microRNAs as Prognostic Biomarkers in Laryngeal Carcinoma.International journal of molecular sciences · 2024Review
- The crosstalk between non-coding RNAs and cell-cycle events: A new frontier in cancer therapy.Molecular therapy. Oncology · 2024Review
- Article
- A New Approach to Melanoma Treatment: microRNAs.Current topics in medicinal chemistry · 2024Review
- Role of miRNA in Melanoma Development and Progression.International journal of molecular sciences · 2022Review
- Mechanism and Role of Endoplasmic Reticulum Stress in Osteosarcoma.Biomolecules · 2022Review
- Deficiency of miRNA-149-3p shaped gut microbiota and enhanced dextran sulfate sodium-induced colitis.Molecular therapy. Nucleic acids · 2022Article
- Harmine reinforces the effects of regorafenib on suppressing cell proliferation and inducing apoptosis in liver cancer cells.Experimental and therapeutic medicine · 2022Article
- Evaluation of a Dual PI3K/mTOR Inhibitor PF-04691502 against Bladder Cancer Cells.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Article
- Review
- Long non-coding RNA MEG3 mediates the miR-149-3p/FOXP3 axis by reducing p53 ubiquitination to exert a suppressive effect on regulatory T cell differentiation and immune escape in esophageal cancer.Journal of translational medicine · 2021Article
- The glycocalyx core protein Glypican 1 protects vessel wall endothelial cells from stiffness-mediated dysfunction and disease.Cardiovascular research · 2021Article
- ITIH5, a p53-responsive gene, inhibits the growth and metastasis of melanoma cells by downregulating the transcriptional activity of KLF4.Cell death & disease · 2021Article
- Biological relevance and therapeutic potential of G-quadruplex structures in the human noncoding transcriptome.Nucleic acids research · 2021Review
40 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
13 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor p53 is activated in response to cellular stress to prevent malignant transformation by activation of the DNA repair machinery to preserve the cell, or by induction of apoptosis to eliminate the cell should the damage prove irrevocable. The gene encoding p53 frequently undergoes inactivating mutations in many human cancers, but WT p53 is often expressed at high levels in melanoma, which, as judged from the malignant nature of the disease, fails to act as an effective tumor suppressor. Here we show that p53 directly up-regulates microRNA-149* (miR-149*) that in turn targets glycogen synthase kinase-3α, resulting in increased expression of Mcl-1 and resistance to apoptosis in melanoma cells. Although deficiency in miR-149* undermined survival of melanoma cells and inhibited melanoma growth in a mouse xenograft model, elevated expression of miR-149* was found in fresh human metastatic melanoma isolates, which was associated with decreased glycogen synthase kinase-3α and increased Mcl-1. These results reveal a p53-dependent, miR-149*-mediated pathway that contributes to survival of melanoma cells, provides a rational explanation for the ineffectiveness of p53 to suppress melanoma, and identifies the expression of miR-149* as a mechanism involved in the increased expression of Mcl-1 in melanoma cells.
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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.