ArticlePloS one2025
Integrated analysis of ARHGAP6 potential function and prognostic value in acute myeloid leukemia.
Article in PloS one, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLeukemia recurrence continues to be the primary cause of treatment failure, it is meaningful to find new biomarkers for its treatment. In this study, we aim to use cell line study to assess the expression and prognostic value of ARHGAP6 in acute myeloid leukemia.
methodsWe applied two acute myeloid leukemia cell lines in the research. Expression level, proliferation assay and apoptosis assay for ARHGAP6 in those cell lines were involved for the study. Then, GEO, TCGA data and bioinformatics analysis were evaluated.
resultsTHP-1 and U937 cell lines both had higher expression levels of ARHGAP6 than control. The cell proliferation of THP-1 and U937 transfected with ARHGAP6 siRNA was significantly reduced. Knock down the gene ARHGAP6 increases AML cell apoptosis. The overall survival (OS) and disease-free survival (DFS) was assessed against the expression of ARHGAP 6 using the KM plotter databases. High expression ARHGAP6 was associated poor OS and DFS in AML. Enrichment analysis suggested that ARHGAP6 mainly mediated the function of growth factor binding, immunoglobulin binding, mRNA binding. Involved in LCK proto-oncogene, Src family tyrosine kinase, tyrosine kinase non receptor 2, platelet derived growth factor receptor beta and Rho associated coiled-coil containing protein kinase 1.
conclusionFrom cell lines-based functional assays to bioinformatic analysis, this study demonstrated that clinical potential of ARHGAP6 as a novel biomarker of AML.
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.