ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
LncRNA MKLN1-AS promotes glioma tumorigenesis and growth via activating the Hippo pathway through miR-126-5p/TEAD1 axis.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. 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
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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.
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.
- Research progress on glioma drug resistance: mechanism analysis and therapeutic strategies.Frontiers in pharmacology · 2026Review
- Mechanism of lncRNA WARS2-IT1 promoting angiogenesis of glioma through miR-299-3P/VEGFA axis and activating PI3K/AKT signaling pathway.Cytotechnology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The involvement of long non-coding RNAs (lncRNAs) in glioma carcinogenesis has gradually been identified. Herein, we aimed to explore the function and mechanism of lncRNA muskelin 1 antisense RNA (MKLN1-AS) in glioma cell oncogenic properties. Quantitative real-time polymerase chain reaction was utilized to test the expression of MKLN1-AS, miR-126-5p, and TEAD1 (TEA Domain Transcription Factor 1) mRNA expression. Oncogenic properties of glioma cells were characterized using 5-ethynyl-2'-deoxyuridine, flow cytometry, wound healing, transwell, and tube formation assays, respectively. Levels of TEAD1 protein, mobility-related proteins, and Hippo pathway-related proteins were examined by Western blotting. The binding between miR-126-5p and MKLN1-AS or TEAD1 was confirmed by using dual-luciferase reporter and pull-down assays. The murine xenograft model was established for in vivo analysis. Levels of MKLN1-AS in glioma tissues and cell lines were higher, functionally, MKLN1-AS deficiency could suppress glioma cell proliferation, migration, invasion, and angiogenesis, and induce apoptosis in vitro, as well as impede tumor growth in vivo. Mechanistically, miR-126-5p was targeted by MKLN1-AS, miR-126-5p directly targeted TEAD1. The suppressing effects of MKLN1-AS deficiency on glioma cell oncogenic properties were abolished by TEAD1 overexpression or miR-126-5p inhibition. Besides, MKLN1-AS/miR-126-5p mediates the activation of Hippo pathway by TEAD1. MKLN1-AS knockdown weakened glioma cell oncogenic phenotypes and growth via TEAD1-Hippo pathway through miR-126-5p, indicating a new therapeutic target for glioma molecular therapy.
Indexed as
Identifiers
39680098What 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.