ArticleJournal of molecular histology2021
miR-4319 inhibited retinoblastoma cells proliferation, migration, invasion and EMT progress via suppressing CD147 mediated MMPs expression.
Article in Journal of molecular histology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 6 citations in OpenAlex.
- Gentiopicroside inhibits retinoblastoma cell proliferation, invasion, and tumorigenesis in nude mice by suppressing the PI3K/AKT pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- CD147: an integral and potential molecule to abrogate hallmarks of cancer.Frontiers in oncology · 2023Review
- Role of non-coding RNAs and exosomal non-coding RNAs in retinoblastoma progression.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor migration is the critical step that lead to the migration in retinoblastoma (RB), in which microRNAs (miRNAs) play important roles. This study aimed to investigate the role of microRNA-4319 (miR-4319) in the development of retinoblastoma by identifying its targets, as well as its underlying regulatory mechanisms. Our data shown that miR-4319 was downregulated in RB tissues and RB cell lines. Enhanced miR-4319 suppressed cell proliferation, migration, invasion and EMT progress, promoted cell apoptosis in SO-RB50 and RB-Y79 cells. Of note, extracellular matrix metalloproteinase inducer (EMMPRI/CD147) was identified as a direct target gene for miR-4319. MMPs were regulated by CD147 and participated in the miR-4319 regulatory network in SO-RB50 cells. In addition, overexpression of CD147 abrogated the inhibitory effect of miR-4319 on RB cells. In summary, miR-4319 overexpression suppressed cell proliferation, migration and invasion may through suppressing the CD147 mediated MMPs expression, suggesting that miR-4319 may serve as a potential diagnostic biomarker and treatment target for RB.
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Registered trials
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