ArticleNon-coding RNA research2026
The regulatory role of circGDI2 in hepatocellular carcinoma proliferation and glycolysis with the involvement of m6A modification.
Article in Non-coding RNA research, 2026. 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Hepatocellular carcinoma (HCC) is a highly aggressive malignancy, and metabolic reprogramming, particularly glycolysis, plays a crucial role in its progression. Circular RNAs (circRNAs) and N6-methyladenosine (m Objective: This study aimed to investigate the functional role and mechanism of circGDI2 in HCC proliferation and glycolysis. Methods: The expression of circGDI2 was detected by RT-qPCR. RNase R treatment was used to verify the stability of circGDI2. Functional assays, including CCK-8, glycolysis analysis (glucose consumption, lactate production), and xenograft model, were performed to assess proliferation and glycolysis. Bioinformatics prediction, MeRIP, and luciferase reporter assays were used to explore the interaction between circGDI2, IGF2BP2, and PKM2. Results: CircGDI2 was highly expressed in HCC tissues and cells, and exhibited cytoplasm localization. Silencing circGDI2 inhibited Li-7 and Huh-7 cell proliferation and glycolysis, downregulated PKM2, and suppressed tumor growth. Mechanistically, circGDI2 regulated PKM2 through the m Conclusions: FTO-mediated m
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.