Evidence map›Paper›PMID 40563399›Full record

ReviewBiomolecules2025

miR-28: A Tiny Player in Cancer Progression and Other Human Diseases.

Karol Kotarski, Marta Kot, Klaudia Skrzypek

Abstract readReview
In one paragraph

Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Karol KotarskiDepartment of Transplantation, Institute of Pediatrics, Faculty of Medicine, Jagiellonian University Medical College, 30-663 Krakow, Poland.ORCID 0009-0009-1215-3518
Marta KotDepartment of Transplantation, Institute of Pediatrics, Faculty of Medicine, Jagiellonian University Medical College, 30-663 Krakow, Poland.ORCID 0000-0002-0602-0411
Klaudia SkrzypekDepartment of Transplantation, Institute of Pediatrics, Faculty of Medicine, Jagiellonian University Medical College, 30-663 Krakow, Poland.ORCID 0000-0002-3997-924X

Funding

Jagiellonian University Medical College N41/DBS/000851; N41/DBS/001344
6 · The paper itself

Abstract

MicroRNAs belong to a class of small non-coding RNA molecules that regulate gene expression post-transcriptionally. By binding to specific mRNA sequences, microRNAs can either inhibit translation or promote transcript degradation. MicroRNA-28 (miR-28) plays a pivotal role in regulating the processes responsible for the pathogenesis of numerous diseases. Its function is contingent upon the specific type of disease and the cellular microenvironment. miR-28 can act as both an inhibitor and inducer of pathogenic processes. This article discusses the impact of miR-28 on the progression of various types of cancer, with particular emphasis on its role as a regulator of gene expression involved in cell proliferation, apoptosis, invasion, migration, and metastasis. Additionally, the article delves into the role of miR-28 in other human diseases and its influence on the processes that underlie their development. A comprehensive understanding of the precise mechanisms through which this specific microRNA exerts its regulatory functions could significantly impact the development of novel therapies. Furthermore, there is potential for miR-28 to be utilized as a diagnostic and preventative biomarker.

Indexed as

MicroRNAsNeoplasmsAnimalsApoptosisCell MovementCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMicroRNAsMIRN28 microRNA, humanbiomarkercancercircRNAlncRNAmetastasismiR-28miRNAnon-coding RNAoncogeneoncomiR

Identifiers

PMID40563399
PMCPMC12191195

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.