ArticleOncology letters2019
Mechanism of miR-107-targeting of regulator of G-protein signaling 4 in hepatocellular carcinoma.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Exploring senescence as a modifier of β cell extracellular vesicles in type 1 diabetes.Frontiers in endocrinology · 2024Review
- RGS proteins and their roles in cancer: friend or foe?Cancer cell international · 2023Review
- Long non-coding RNA H19 promotes proliferation in hepatocellular carcinoma cells via H19/miR-107/CDK6 axis.Oncology research · 2023Article
- Tackling cellular senescence by targeting miRNAs.Biogerontology · 2022Review
- Identification of Novel Imatinib-Resistant Genes in Gastrointestinal Stromal Tumors.Frontiers in genetics · 2022Article
- Review
- The Epigenetic Regulation of Microenvironment in Hepatocellular Carcinoma.Frontiers in oncology · 2021Review
- NKX2-1 re-expression induces cell death through apoptosis and necrosis in dedifferentiated thyroid carcinoma cells.PloS one · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the mechanism of microRNA (miR)-107 in targeting regulator of G-protein signaling 4 (RGS4) in hepatic carcinoma. SK-HEP-1 cells were transfected with miR-107 mimics and control mimics. Reverse transcription-quantitative PCR was performed to determine the miR-107 expression levels, and following miR-107 upregulation, MTT, colony formation, transwell and wound-healing assays were performed to assess cell proliferation, colony-forming ability, invasion and migration, respectively. In addition, the effect of miR-107 upregulation on the cell cycle and apoptosis in SK-HEP-1 cells was evaluated using flow cytometry. Western blot analysis was performed to measure the protein expression levels of RGS4, epidermal growth factor receptor (EGFR), CXC chemokine receptor type 4 (CXCR4) and matrix metalloproteinase (MMP)-2 and -9. Expression level changes and the association between miR-107 and RGS4 in HCC cells were assessed using dual luciferase analysis. The results indicated that the overexpression of miR-107 in HCC cells suppressed cellular proliferation, invasion, migration and colony-forming ability, but promoted apoptosis and G
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Registered trials
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