ArticleOncology letters2020
MicroRNA-505-3p inhibits development of glioma by targeting HMGB1 and regulating AKT expression.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 8 citations in OpenAlex.
- Targeting Immune Checkpoint Proteins in Cancer Therapy and the Potential of RNAi-Based Immunotherapy.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Hypoxia-Regulated Tumor-Derived Exosomes and Tumor Progression: A Focus on Immune Evasion.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have reported that microRNA (miR)-505 exhibits important effect in human cancers. However, the regulatory mechanism of miR-505-3p/high-mobility group box 1 (HMGB1) axis is still unclear in glioma. Therefore, the regulatory mechanism of miR-505-3p/HMGB1 axis in glioma was illuminated. Expression of miR-505-3p and HMGB1 was observed by RT-qPCR. Protein expression was measured by western blot analysis. Dual luciferase assay was performed to confirm the relationship between miR-505-3p and HMGB1. The function of miR-505-3p was investigated by MTT and Transwell assays. Expression of miR-505-3p was reduced in glioma, which was related to poor clinical outcomes and prognosis in glioma patients. Moreover, overexpression of miR-505-3p suppressed proliferation, migration and invasion of glioma cells. In addition, HMGB1 was confirmed as a direct target of miR-505-3p, and miR-505-3p inhibited the development of glioma by targeting HMGB1. Furthermore, miR-505-3p blocked EMT suppressing p-AKT expression in glioma cells. In conclusion, miR-505-3p inhibited the development of glioma by targeting HMGB1 and regulating AKT expression.
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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.