ArticleEuropean journal of medical research2025
LncRNA AC116914.2 promotes the progression of oral cancer by targeting METTL3 via miR-1245a/ZNF250.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundAberrant long non-coding RNA (lncRNA) expression regulates tumor progression. With rising incidence, oral squamous cell carcinoma (OSCC) requires mechanistic study. LncRNA functions in OSCC remain unclear.
methodsBioinformatics analysis was conducted to screen the highly expressed lncRNA AC116914.2 associated with m6A methylation in OSCC from The Cancer Genome Atlas database. Techniques including IHC, Western Blot, qPCR, cell functional assays, and in-vivo tumor formation were applied to assess the effects of AC116914.2 on OSCC malignant behaviors and fibroblast functions. Dual-luciferase assays explored the interactions among AC116914.2, miR-1245a, and ZNF250, while ChIP-qPCR verified ZNF250's regulatory effect on METTL3.
resultsLncRNA AC116914.2 showed differential expression between tumor and normal tissues. Its knockdown significantly inhibited OSCC progression in vitro and in vivo. Mechanistically, AC116914.2 competitively bound to miR-1245a to maintain ZNF250 levels, stabilizing the oncogene METTL3 expression. Additionally, AC116914.2 promoted extracellular vesicle release and activated cancer-associated fibroblasts, fostering an OSCC-favorable microenvironment.
conclusionThis study shows that lncRNA AC116914.2, as a competing endogenous RNA (ceRNA), regulates the expression of METTL3 by competitively binding to miR-1245a with ZNF250, thus promoting OSCC progression. The discovery of this regulatory axis provides new diagnostic markers and therapeutic targets for OSCC.
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.