ArticleCell biochemistry and biophysics2025
Micro-RNA-140-3p Acts as a Tumor Suppressor Gene in Acute Promyelocytic Leukemia by Targeting Hepatocyte Growth Factor.
Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper 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
9 authors.
Funding
Abstract
MicroRNAs (miRNAs) are noncoding RNAs that regulate the expression of target genes after transcription, and play important roles in the differentiation of hematopoietic stem cells. Many miRNAs are related to the occurrence of acute promyelocytic leukemia (APL) and play roles in the treatment response. Recently, we demonstrated that several miRNAs are differentially expressed in patients with relapsed and newly diagnosed APL; for example, miR-140-3p is significantly downregulated in patients with relapsed APL. In this study, via a dual luciferase assay, we verified that one of the direct target genes of miR-140-3p is hepatocyte growth factor (HGF). After different lentiviruses were transfected into NB4 cells, and flow cytometry and proliferation assays confirmed that low expression of miR-140-3p inhibited the differentiation and apoptosis of NB4 cells and induced proliferation by promoting cell cycle progression. In summary, our findings suggest that hepatocyte growth factor is a target gene of miR-140-3p. Moreover, upregulation of miR-140-3p expression in APL cells inhibits cell proliferation, arrests cell cycle progression, and promotes apoptosis and cell differentiation. Monitoring the levels of miR-140-3p and HGF may predict the risk of disease recurrence, and interfering with the miR-140-3p / HGF pathway may have therapeutic potential for treating recurrent APL.
Indexed as
Identifiers
40057668What 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.