Evidence map›Paper›PMID 42056342›Full record

ArticleDiscover oncology2026

Integrative bioinformatics and molecular simulations identify HMGB3 as a key immune modulator in triple negative breast cancer.

Uma Chaudhary, Mythili Asaithambi

Abstract read
In one paragraph

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

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

2 authors.

Uma ChaudharyDepartment of Biotechnology, School of Biosciences and Technology, Vellore Institute of Technology (VIT), Vellore, Tamil Nadu, 632014, India.ORCID http://orcid.org/0000-0002-0172-5172
Mythili AsaithambiDepartment of Sensor and Biomedical Technology, School of Electronics Engineering, Vellore Institute of Technology (VIT), Vellore, Tamil Nadu, 632014, India. mythili.asaithambi@vit.ac.in.ORCID http://orcid.org/0000-0003-1993-0817

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTriple-negative breast cancer is an aggressive and its diverse subtype that lacks targeted treatment options and often shows resistance to immune-based therapies. This study aimed to identify immune-related regulatory axes within BLIA and MLIA subtypes by integrating ceRNA network of ncRNAs and mRNAs, and to evaluate HMGB3 as a potential therapeutic target.

methodsTranscriptomic datasets from GEO and TCGA were analyzed to identify DE-mRNAs. Network analysis was performed using STRING, CytoHubba, CytoNCA, and MCODE in Cytoscape. HMGB3-associated ncRNAs were examined for functional relevance. Molecular docking, ADMET evaluation, and molecular dynamics (MD) simulations were conducted to assess ligand binding and complex stability.

resultsHMGB3 showed strong association with poor prognosis in MLIA subtype. The HMGB3-miR-214-3p-let-7f-5p-NEAT1 axis emerged as a potential immune-modulatory pathway. Docking revealed high affinity for Pimicotinib (- 8.0 kcal/mol), CID17584963 (7.0 kcal/mol), and CID1763476 (kcal/mol). MD simulations confirmed the stability of these complexes, reflected by lower RMSD, reduced residue fluctuations, compact conformations, and decreased solvent exposure.

conclusionThis work identifies HMGB3 as a promising immunotherapeutic target in the MLIA subtype of TNBC and highlights Pimicotinib, CID17584963, and CID1763476 as potential HMGB3 inhibitors for drug repurposing strategies.

Indexed as

BiomarkerBreast cancerDrug resistanceHMGB3Immunotherapy

Identifiers

PMID42056342
PMCPMC13272729

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

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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.