ArticleFrontiers in pharmacology2026
CircHIPK3 promotes the progression of B-cell acute lymphoblastic leukemia in children by binding to STAT3.
Article in Frontiers in pharmacology, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Circular RNAs (circRNAs) have emerged as critical post-transcriptional regulators in hematological malignancies; however, the specific role and molecular mechanism of circHIPK3 in pediatric B-cell acute lymphoblastic leukemia (B-ALL) remain unexplored. Methods: circHIPK3 expression was profiled in clinical B-ALL specimens and cell lines. The biological functions were evaluated using CCK-8, flow cytometry, and Results: CircHIPK3 was aberrantly upregulated in B-ALL tissues and cells, exhibiting exceptional stability and predominant cytoplasmic localization. CircHIPK3 silencing significantly impaired leukemic cell proliferation, induced G0/G1 cell cycle arrest, and triggered apoptosis. Mechanistically, we identified a direct physical association between cytoplasmic circHIPK3 and STAT3. CircHIPK3 did not alter STAT3 transcription but rather acted as a protein scaffold that shielded STAT3 from ubiquitin-mediated proteasomal degradation, thereby enhancing its protein stability. Ectopic STAT3 expression reversed the tumor-suppressive phenotypes caused by circHIPK3 deficiency. Consistently, circHIPK3 knockdown attenuated leukemic infiltration in xenograft mice. Conclusion: Our findings characterize circHIPK3 as a potent oncogenic driver in B-ALL that functions by stabilizing STAT3 via the ubiquitin-proteasome pathway. Targeting the circHIPK3/STAT3 axis may represent a potential therapeutic strategy for B-ALL treatment.
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.