ReviewClinical and experimental medicine2025
Regulation and function of microRNA-152 in various types of cancers: its upstream regulators and downstream targets.
Review in Clinical and experimental medicine, 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.
- miR-152-3p Overcomes Temozolomide Resistance in Glioblastoma by Targeting TGF-α and Enhancing Apoptosis.Oncology research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) are key regulators of gene expression that bind to the 3'-untranslated region (3'-UTR) of target mRNAs, modulating protein expression and influencing cancer progression. Among these, microRNA-152 (miR-152) is frequently downregulated in diverse malignancies-including breast, endometrial, gastrointestinal, and hematologic cancers-primarily due to promoter hypermethylation. This epigenetic silencing, mediated by DNMT1, is compounded by competitive sponging from long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs), forming intricate regulatory networks. Functionally, miR-152 acts as a tumor suppressor by targeting oncogenic pathways such as PI3K/AKT/mTOR, EMT drivers, and chemoresistance mediators. However, its role is context-dependent, exhibiting dual oncogenic and suppressive effects in prostate cancer and certain leukemias. Therapeutically, restoring miR-152 expression via mimics, demethylating agents, or nanocarrier-based delivery systems shows promise in preclinical studies for reversing chemoresistance and inhibiting metastasis. This review synthesizes miR-152's upstream regulators, downstream targets, and clinical potential, offering a roadmap for its exploitation in precision oncology.
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What Socratic 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 Socratic graph.