ArticleOncotarget2017
MiR-520f promotes cell aggressiveness by regulating fibroblast growth factor 16 in hepatocellular carcinoma.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Fibroblast growth factor 16: Molecular mechanisms, signalling crosstalk, and emerging roles in cardiac biology and metabolic regulation.Pharmacological research · 2025Review
- Pathology and Therapeutic Significance of Fibroblast Growth Factors.Targets (Basel) · 2025Article
- Fibroblast Growth Factors: Roles and Emerging Therapeutic Applications.Current drug targets · 2025Review
- Decoding FGF/FGFR Signaling: Insights into Biological Functions and Disease Relevance.Biomolecules · 2024Review
- Comprehensive in silico analysis of prognostic and immune infiltrates for FGFs in human ovarian cancer.Journal of ovarian research · 2024Article
- Reprogramming of glucose metabolism via PFKFB4 is critical in FGF16-driven invasion of breast cancer cells.Bioscience reports · 2023Article
- FGF16 regulated by miR-520b enhances the cell proliferation of lung cancer.Open medicine (Warsaw, Poland) · 2021Article
- MicroRNA-3690 promotes cell proliferation and cell cycle progression by altering DKK3 expression in human thyroid cancer.Oncology letters · 2020Article
- Functional analysis of miR-767-5p during the progression of hepatocellular carcinoma and the clinical relevance of its dysregulation.Histochemistry and cell biology · 2020Article
- MicroRNA-7 inhibits hepatocellular carcinoma cell invasion and metastasis by regulating Atg5-mediated autophagy.Translational cancer research · 2020Article
- miR-455 Functions as a Tumor Suppressor Through Targeting GATA6 in Colorectal Cancer.Oncology research · 2019Article
- Overexpressing lncRNAOncoTargets and therapy · 2018Article
- Prospects of Noncoding RNAs in Hepatocellular Carcinoma.BioMed research international · 2018Review
Corrections and comments
- Retraction · 2025-12-31Duplication of/in Image · Euphemisms for Plagiarism · Investigation by Journal/Publisher · Plagiarism of Image ·
- Retracted
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer metastasis is a multistep cellular process, which has be confirmed one of mainly causes of cancer associated-death in hepatocellular carcinoma (HCC). MicroRNAs (miRNAs) participate in tumorigenesis function as either tumor suppressor genes or oncogenes. In order to elaborate the critical miRNAs and their targets in HCC, we compared the differential expression of miRNA between HCC tissues and normal tissues. Microarray analysis revealed there were several significantly up-expression miRNAs in HCC, compared to normal solid tissue. Among them, the expression of miR-520f was the most over-expression in HCC cell lines than that in human normal liver cells LO2, as well as up-regulated in HCC than that in the corresponding normal tissues. Moreover, Kaplan Meier-plotter analyses revealed that higher miR-520f levels were negatively correlated with poor overall survival. By applying bioinformatics methods to identify the targeting genes of miRNA, we demonstrated that fibroblast growth factor 16 (FGF16) was the miR-520f-targeted gene. Meanwhile, FGF16 exhibited similar expression patterns to miR-520f in HCC. Forced miR-520f expression accelerated HCC cells proliferation and aggressiveness
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What OpenQuestion holds
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.