ArticleAnnals of hematology2025
Down-regulation of circMUC16 inhibited the progression of ALL via interaction with miR-1182 and TPPP3.
Article in Annals of hematology, 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
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
2 citing papers in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Circular RNA (circRNA) is crucial in various biological processes, particularly in the onset and progression of different diseases. Nevertheless, the function of circMUC16 in acute lymphoblastic leukemia (ALL) remains unclear. The expression of circMUC16, miR-1182 and TPPP3 was evaluated by qPCR. The role of circMUC16 in the progression of ALL was investigated bymcherry-EGFP-LC-3, cell cycle, flow cytometry apoptosis, caspase-3 activity, western blotting, and an in vivo xenograft model. The interactions among circMUC16, miR-1182, and TPPP3 were explored by using qPCR, western blot, dual-luciferase reporter, and RNA immunoprecipitation assays.In this study, it was found that circMUC16 was increased in ALL cells. Down-regulation of circMUC16 reduced autophagy, cell proliferation and increased apoptosis in vitro while inhibiting cancer in vivo. circMUC16 acted as a molecular sponge of miR-1182. The carcinogenic effect of circMUC16 was partially mediated by miR-409-3p. TPPP3 was shown to be a direct target of miR-1182 and to be competed with circMUC16. Overexpression of TPPP3 partially counteracted the inhibitory effects of sh-circMUC16 inhibition on malignant behaviors of ALL cells. This study revealed that the circMUC16/miR-1186/TPPP3 axis plays a crucial role in the progression of ALL, suggesting a novel therapeutic target for ALL therapy.
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.