ArticleNeurotoxicity research2022
MIR99AHG/miR-204-5p/TXNIP/Nrf2/ARE Signaling Pathway Decreases Glioblastoma Temozolomide Sensitivity.
Article in Neurotoxicity research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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
6 citing papers in PubMed, 8 citations in OpenAlex.
- Long Non-Coding RNAs in Malignant Human Brain Tumors: Driving Forces Behind Progression and Therapy.International journal of molecular sciences · 2025Review
- Analysis of the expression of ARNTL2 and miR-204-5p and their correlation with clinical pathological features in NSCLC patients.American journal of clinical and experimental immunology · 2025Article
- MicroRNA-204-5p Ameliorates Renal Injury via Regulating Keap1/Nrf2 Pathway in Diabetic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Identification of glioblastoma stem cell-associated lncRNAs using single-cell RNA sequencing datasets.Stem cell reports · 2023Article
- Article
- Recent advances in ferroptosis and therapeutic strategies for glioblastoma.Frontiers in molecular biosciences · 2022Review
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
Glioblastoma (GBM) is the most prevalent primary cerebral tumor in adults with high aggressiveness. Temozolomide (TMZ) is considered as the most widely used chemotherapy for GBM patients. Accumulating studies have proved that long non-coding RNAs (lncRNAs) participate in the pathogenesis of tumors. The aim of our study is to disclose the role of mir-99a-let-7c cluster host gene (MIR99AHG) in GBM. MIR99AHG expression was discovered to be elevated in GBM cells through quantitative real-time polymerase chain reaction (RT-qPCR) analysis. Loss-of-function experiments demonstrated that MIR99AHG silencing enhanced TMZ sensitivity of GBM both in vitro and in vivo. RNA pull down, RNA-binding protein immunoprecipitation (RIP), and luciferase reporter assays were implemented to unveil the underlying mechanism of MIR99AHG in GBM. The results of the mechanism assays implied that MIR99AHG interacted with microRNA-204-5p (miR-204-5p) and enhanced thioredoxin interacting protein (TXNIP) expression to inactivate the Nrf2/ARE signaling pathway. MIR99AHG/miR-204-5p/TXNIP regulatory axis was verified by rescue experiments in GBM. To summarize, MIR99AHG plays a promoting role in the TMZ resistance of GBM cells. The findings in this study might provide novel sight for the treatment for GBM.
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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 Socratic graph.