ArticleDiscover oncology2025
The expression of miR-381-3p in acute myeloid leukemia and its effect on corresponding cell proliferation and apoptosis.
Article in Discover oncology, 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo investigate the expression, clinical significance, progression, and prognosis of miR-381-3p in acute myeloid leukemia (AML), as well as its impact on AML cell proliferation and apoptosis, in order to provide theoretical basis for the treatment of AML.
methodUsing bioinformatics analysis to identify differentially expressed miRNAs, clinical data and blood samples of AML patients were collected, and the expression levels of miRNAs in the bone marrow fluid of the included patients were measured to further elucidate the relationship between miRNAs and AML. The included patients were followed up to calculate overall survival (OS) and disease-free survival (DFS); In vitro cultivation of AML cells, construction of miR-381-3p plasmids, overexpression of miR-381-3p and knockdown of miR-381-3p in AML, divided into five groups: control, miR-381 mimics, mimics NC, miR-381 inhibitor, inhibitor NC. The proliferation and apoptosis of AML cells were detected using CCK-8 and flow cytometry.
resultsDifferentially expressed miRNAs were identified using bioinformatics analysis, and miR-381-3p was ultimately determined as the study molecule. A total of 90 AML patients were included. The expression level of miR-381 in AML patients was lower than that in the control group, and all FAB subtypes were lower than that in the normal group; The expression level of miR-381 is not related to the age, gender, peripheral blood leukocytes, lymphocytes, and FAB typing of AML patients, and the OS and PFS of miR-381 patients with high expression are significantly prolonged, with statistically significant differences; In vitro experiments have shown that knocking down miR-381 can inhibit apoptosis and promote proliferation of AML cells. Overexpression of miR-381 can promote apoptosis and inhibit proliferation of AML cells.
conclusionmiR-381-3p is low expressed in AML patients, and its overexpression can significantly prolong OS and PFS. miR-381-3p can promote apoptosis of AML cells, inhibit proliferation, and may become a targeted molecule for the treatment 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.