ReviewHeliyon2024
New sights on long non-coding RNAs in glioblastoma: A review of molecular mechanism.
Review in Heliyon, 2024. 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
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
6 citing papers in PubMed.
- Identification of hub mRNAs and long non-coding RNAs involved in temozolomide-resistant glioblastoma (brain cancer) cell lines.Discover oncology · 2026Article
- From Integrated Analysis to Clinical Insight: ncRNA-Mediated Ferroptosis in Glioblastoma.Cancers · 2026Review
- Role of HOXA transcript antisense RNA myeloid-specific 1 in cancer (Review).Oncology letters · 2026Review
- Long non-coding RNAs in glioblastoma: from molecular drivers to therapeutic targets.Frontiers in immunology · 2026Review
- MALAT1 Expression Is Deregulated in miR-34a Knockout Cell Lines.Non-coding RNA · 2025Article
- Key genes altered in glioblastoma based on bioinformatics (Review).Oncology letters · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioma or glioblastoma (GBM) is one of the aggressive and fatal primary cerebral malignancies, with the highest mortality rate among all brain-related tumors. Also, glioma mainly progresses as a more invasive phenotype after primary treatment. Cumulative evidence suggested that dysregulation of noncoding RNAs (ncRNAs) such as long non-coding RNAs (LncRNAs) and microRNAs (miRNAs) are associated with tumor initiation, progression, and drug resistance, through epigenetic modifications, transcriptional, and post-transcriptional processes in the cells. Many scientific investigations have revealed that LncRNAs play important roles in various biological procedures linked with the development and progression of GBM. In recent years, it has been shown that dysregulation of molecular mechanisms in many LncRNAs such as MIR22HG, HULC, AGAP2-AS1, MALAT1, PVT1, TTTY14, HOTAIRM1, PTAR, LPP-AS2, LINC00336, and TINCR are connected with the GBM. Therefore, this scientific review paper focused on the molecular mechanisms of these LncRNAs in the context of GBM.
Indexed as
Identifiers
What Socratic 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 Socratic graph.