Evidence map›Paper›PMID 41735610›Full record

ArticleMedical oncology (Northwood, London, England)2026

FN1 as a key gene in modulating the integrin cell surface pathway in breast cancer.

Mahboubeh Sadeghi, Abbas Ghaderi, Pegah Mousavi, Soudabeh Sabetian, Amin Ramezani, Mohammad Reza Haghshenas

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

6 authors.

Mahboubeh SadeghiStudent Research Committee, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
Abbas GhaderiDepartment of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. ghaderia@sums.ac.ir.
Pegah MousaviEndocrinology and Metabolism Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran. pegahmousavi2017@gmail.com.
Soudabeh SabetianInfertility Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. soudabehsabet@gmail.com.
Amin RamezaniShiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Mohammad Reza HaghshenasShiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.

Funding

deputy of Research in the Hormozgan University of Medical Sciences, Bandar Abbas, Iran. 4000409
6 · The paper itself

Abstract

Breast carcinoma represents the most prevalent form of invasive neoplasia among the female population globally, and is distinguished by its molecular heterogeneity by significant genomic instability. The discipline of bioinformatics provides essential tools for the identification of novel biomarkers and enhances the prospects for subsequent experimental investigations. Differentially expressed messenger RNAs were assembled by employing datasets sourced from the Gene Expression Omnibus repository. Intersection of DEGs and proteins involving in the integrin cell surface interactions were done. Ce-RNA network were constructed and Functional analysis were done. Protein expression analysis, methylation and, Correlation analysis as well as drug sensitivity analysis for the hub genes were performed. The expression of FN1 were evaluated using Real-Time PCR for 45 invasive ductal carcinoma breast tissues and adjacent normal samples. We found FN1, CDH1, COMP, SPP1 and ITGA7 to act in integrin cell surface interactions. The Ce-RNA network consisted of 126 nodes and 192 edges which the network nodes were significantly enriched in known cancer pathways. Protein expressions of FN1, CDH1, COMP was upregulated while ITGA7 were downregulated. The methylation levels in ITGA7 and SPP1 promoter regions were significantly altered across all stages compared to normal. In contrast, FN1 and CDH1 promoter regions exhibited dysregulation only in stage 3 relative to normal. A correlation study identified five positive and three negative gene correlations. Altered expression of FN1, SPP1, CDH1, and ITGA7 in breast cancer enhanced cancer cell susceptibility to specific pharmacological molecules. FN1 expression was markedly higher in breast cancer tissues compared to non-cancerous tissues, showing a threefold increase (p < 0.0001). Both early-stage and advanced-stage cancers showed higher FN1 levels (p = 0.002, p = 0.01). Additionally, FN1 was higher in lower histological grade tissues (p = 0.0002). In ROC curve analysis with limited stage III samples, FN1 showed potential for diagnosing IDC, achieving an AUC of 0.82. We identified FN1 as a highly connected component of integrin cell-surface interactions in breast cancer and provide hypothesis-generating associations with drug sensitivity; these findings require further protein-level validation and functional testing before translational application.

Indexed as

Breast NeoplasmsCarcinoma, Ductal, BreastFibronectinsIntegrinsAntigens, CDBiomarkers, TumorCadherinsDNA MethylationFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansIntegrin alpha ChainsOsteopontinPromoter Regions, GeneticAntigens, CDBiomarkers, TumorCadherinsCDH1 protein, humanFibronectinsFN1 protein, humanIntegrin alpha ChainsIntegrinsOsteopontinSPP1 protein, humanBioinformaticsBreast cancerFN1IntegrinReal-Time PCR

Identifiers

PMID41735610

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.