Evidence map›Paper›PMID 42814286›Full record

ArticleMolecular biology reports2026

DNA damage response associated miRNA dysregulation in Ataxia-telangiectasia.

Muhammad Junaid Iqbal, Cecilia Bucci, Anastasia Ricci, Gianluca Morganti, Faez Iqbal Khan, Muhammad Jawad Khan, Michele Menotta

Abstract read
In one paragraph

Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Muhammad Junaid IqbalDepartment of Biomolecular Sciences, University of Urbino "Carlo Bo", Via Saffi 2, 61029, Urbino (PU), Italy. m.iqbal@campus.uniurb.it.ORCID http://orcid.org/0000-0003-3916-6414
Cecilia BucciDepartment of Biomolecular Sciences, University of Urbino "Carlo Bo", Via Saffi 2, 61029, Urbino (PU), Italy.
Anastasia RicciDepartment of Biomolecular Sciences, University of Urbino "Carlo Bo", Via Saffi 2, 61029, Urbino (PU), Italy.
Gianluca MorgantiDepartment of Biomolecular Sciences, University of Urbino "Carlo Bo", Via Saffi 2, 61029, Urbino (PU), Italy.
Faez Iqbal KhanCentre of Excellence for Oncology and Immunology, Academy of Life and Natural Sciences, Xi'an Jiaotong-Liverpool University, No. 111 Ren'ai Road, Suzhou, 215123, China.
Muhammad Jawad KhanDepartment of Biosciences, COMSATS University Islamabad, Park Road, Tarlai Kalan, Islamabad, 45550, Pakistan. jawadkhan@comsats.edu.pk.ORCID http://orcid.org/0000-0002-9570-1517
Michele MenottaDepartment of Biomolecular Sciences, University of Urbino "Carlo Bo", Via Saffi 2, 61029, Urbino (PU), Italy. michele.menotta@uniurb.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtaxia-telangiectasia (A-T) is a rare autosomal recessive genome-instability disorder due to pathogenic variants in ATM, a central kinase of the DNA double-strand break signaling, checkpoint activation and stress-response pathways. Although microRNAs (miRNAs) regulate DNA damage response (DDR), apoptosis, senescence and cell-cycle control, the stress-responsive behavior of selected ATM/DDR-associated miRNAs remains incompletely characterized in A-T fibroblast models. METHODS AND

resultsFour predefined ATM/DDR-associated candidate miRNAs (hsa-miR-34a-5p, hsa-miR-26a-5p, hsa-miR-106b-5p and hsa-miR-20a-5p) were quantified in one ATM-proficient fibroblast control and three A-T fibroblast cell lines both under basal and bleomycin exposed conditions. The relative expression of selected miRNAs was measured by RT-qPCR. miR-34a-5p and miR-26a-5p levels were lower in each of the three bleomycin-treated A-T lines relative to the single bleomycin-treated WT control line. miR-34a-5p and miR-26a-5p levels were lower in bleomycin-treated three A-T lines relative to the single control WT line. Within-cell-line analysis showed significant miR-34a-5p induction after bleomycin in WT, AT648 and AT9607, whereas significant miR-26a-5p induction was observed only in AT648. AT648 showed the broadest within-cell-line response, with significant induction of all four tested miRNAs after bleomycin. Target-based enrichment and network analyses of the predefined candidate panel identified annotations related to cell-cycle regulation, G1/S transition, RB/E2F signaling, p53 signaling, apoptosis, senescence, PI3K-Akt signaling, and DNA damage-associated processes. Network analysis revealed a number of shared candidate targets such as CCND1, CCND2, E2F1, E2F3, RB1, WEE1, PTEN, SMAD4, MYC and VEGFA.

conclusionsIn this fibroblast panel, miR-34a-5p and miR-26a-5p showed the most consistent baseline alterations, whereas bleomycin responsiveness was cell-line specific and heterogeneous.

Indexed as

Ataxia TelangiectasiaDNA DamageMicroRNAsApoptosisAtaxia Telangiectasia Mutated ProteinsBleomycinCell LineFibroblastsGene Expression RegulationHumansSignal TransductionAtaxia Telangiectasia Mutated ProteinsATM protein, humanBleomycinMicroRNAsMIRN26 microRNA, humanMIRN34 microRNA, humanAtaxia TelangiectasiaATMDNA DamageMicroRNAmiR-26a-5pmiR-34a-5p

Identifiers

PMID42814286
PMCPMC13627277

What OpenQuestion holds

Textmetadata
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.