ArticleOncotarget2014
STAT3 inhibition suppresses proliferation of retinoblastoma through down-regulation of positive feedback loop of STAT3/miR-17-92 clusters.
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, 46 citations in OpenAlex.
- Oligonucleotide-Based Therapeutics for STAT3 Targeting in Cancer-Drug Carriers Matter.Cancers · 2023Review
- Inhibition of protein arginine deiminase II suppresses retinoblastoma in orthotopic transplantation in mice.Oncology reports · 2023Article
- The Role of Non-Coding RNAs in Chromosomal Instability in Cancer.The Journal of pharmacology and experimental therapeutics · 2023Review
- UBE2T/STAT3 Signaling Promotes the Proliferation and Tumorigenesis in Retinoblastoma.Investigative ophthalmology & visual science · 2022Article
- LncRNA MIR17HG promotes the proliferation, migration, and invasion of retinoblastoma cells by up-regulating HIF-1α expression via sponging miR-155-5p.The Kaohsiung journal of medical sciences · 2022Article
- Applications of Non-Coding RNAs in Patients With Retinoblastoma.Frontiers in genetics · 2022Review
- Article
- GNAQ knockdown promotes bone metastasis through epithelial-mesenchymal transition in lung cancer cells.Bone & joint research · 2021Article
- A decision process for drug discovery in retinoblastoma.Investigational new drugs · 2021Article
- MIR17HG polymorphism (rs7318578) is associated with liver cancer risk in the Chinese Han population.Bioscience reports · 2020Article
- Long noncoding RNA SNHG14 promotes the aggressiveness of retinoblastoma by sponging microRNA‑124 and thereby upregulating STAT3.International journal of molecular medicine · 2020Article
- Long noncoding RNAAging · 2020Article
- Silencing UHRF1 Inhibits Cell Proliferation and Promotes Cell Apoptosis in Retinoblastoma Via the PI3K/Akt Signalling Pathway.Pathology oncology research : POR · 2020Article
- Biomarkers in retinoblastoma.International journal of ophthalmology · 2020Review
- Development of a patient-derived xenograft model of glioblastoma via intravitreal injection in mice.Experimental & molecular medicine · 2019Article
- Non-Coding RNAs in Pediatric Solid Tumors.Frontiers in genetics · 2019Review
- Therapeutic Implication of SOCS1 Modulation in the Treatment of Autoimmunity and Cancer.Frontiers in pharmacology · 2019Review
- Targeting STAT3 induces apoptosis and suppresses cell growth and invasion by inactivation of Slug signaling in retinoblastoma.International journal of clinical and experimental pathology · 2018Article
- Article
- GZD824 suppresses the growth of human B cell precursor acute lymphoblastic leukemia cells by inhibiting the SRC kinase and PI3K/AKT pathways.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinoblastoma, the most common intraocular malignant tumor in children, is characterized by the loss of both functional alleles of RB1 gene, which however alone cannot maintain malignant characteristics of retinoblastoma cells. Nevertheless, the investigation of other molecular aberrations such as matrix metalloproteinases (MMPs) and miRNAs is still lacking. In this study, we demonstrate that STAT3 is activated in retinoblastoma cells, Ki67-positive areas of in vivo orthotopic tumors in BALB/c nude mice, and human retinoblastoma tissues of the advanced stage. Furthermore, target genes of STAT3 including BCL2, BCL2L1, BIRC5, and MMP9 are up-regulated in retinoblastoma cells compared to other retinal constituent cells. Interestingly, STAT3 inhibition by targeted siRNA suppresses the proliferation of retinoblastoma cells and the formation of in vivo orthotopic tumors. In line with these results, STAT3 siRNA effectively induces down-regulation of target genes of STAT3. In addition, miRNA microarray analysis and further real-time PCR experiments with STAT3 siRNA treatment show that STAT3 activation is related to the up-regulation of miR-17-92 clusters in retinoblastoma cells via positive feedback loop between them. In conclusion, we suggest that STAT3 inhibition could be a potential therapeutic approach in retinoblastoma through the suppression of tumor proliferation.
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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.