Evidence map›Paper›PMID 42450306›Full record

ArticleInternational journal of molecular sciences2026

Chronic IL-1 Exposure Attenuates IL-1 Response and Alters Gene Expression Regulation While Maintaining Therapeutic Sensitivity in BCa Cell Lines.

Rafah Falah, Roopal Dhar, Stephanie Yamauchi, Monica Bautista, Mohammed Kanchwala, Liu Yan, Dinesh Raju, Linyi Xu, Kylah Reliford, Afshan Nawas and 20 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 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

30 authors.

Rafah FalahDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Roopal DharDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Stephanie YamauchiDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Monica BautistaDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Mohammed KanchwalaBioinformatics Lab, Eugene McDermott Center for Human Growth and Development, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0001-6035-2970
Liu YanBioinformatics Lab, Eugene McDermott Center for Human Growth and Development, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Dinesh RajuBioinformatics Lab, Eugene McDermott Center for Human Growth and Development, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0003-0657-1560
Linyi XuDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0009-0004-3231-5629
Kylah RelifordDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Afshan NawasDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Samrah AliDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Justin FangDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Ola OlaleyeDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Jyotsna TeraDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Rana AbdelazizDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Reshmika KanakalaDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Aniketh SudunaguntaDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Subhash EedarapaliDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Emmalee BurrDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Basir S MansoorDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0009-0007-3581-3422
Nicole RoosDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0000-0003-1142-9331
Sydney DiepDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0000-0002-6898-4443
Hiba AfaqDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Niranjana Pillai RajeshDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Saanvi ManoharDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Jennifer OdikpoDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Abhinav K JainEpigenetics & Molecular Carcinogenesis, Center for Cancer Epigenetics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.ORCID 0000-0003-3268-514X
Zhenyu XuanDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Chao XingBioinformatics Lab, Eugene McDermott Center for Human Growth and Development, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0002-1838-0502
Nikki A DelkDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0000-0001-9482-3830

Funding

American Cancer Society RSG-20-138-01-TBE
6 · The paper itself

Abstract

Chronic inflammation is a hallmark of the breast cancer tumor microenvironment and is also known to be associated with disease progression and therapeutic response. Interleukin-1 (IL-1) signaling has been widely studied in breast cancer biology; however, the long-term effect of sustained IL-1 exposure on hormone receptor-positive breast cancer cells remain poorly understood. In this study, we investigated how chronic IL-1 exposure influences inflammatory response, hormone dependency, and therapeutic sensitivity in ERα+/PR+ breast cancer models, MCF7 and T47D. Chronic IL-1 exposure attenuated response to subsequent acute IL-1 treatment, but the chronically exposed cells remained sensitive to serum deprivation, retained dependence on estrogen or progesterone receptor signaling, and responded robustly to endocrine and chemotherapeutic treatments. Extensive changes in basal gene expression and histone modification revealed that chronic IL-1 exposure alters transcriptional reprogramming and chromatin remodeling. Together, these findings demonstrate that chronic IL-1 signaling drives selective inflammatory response in hormone receptor-positive MCF7 and T47D breast cancer cells. This work underscores the continued therapeutic relevance of hormone receptor-targeted strategies in chronically inflamed tumors and provides insight into how sustained inflammatory stress shapes tumor behavior and gene regulation predicted to promote tumor progression.

Indexed as

Breast NeoplasmsGene Expression Regulation, NeoplasticInterleukin-1Cell Line, TumorEstrogen Receptor alphaFemaleHumansMCF-7 CellsReceptors, ProgesteroneSignal TransductionEstrogen Receptor alphaInterleukin-1Receptors, Progesteroneacute inflammationbreast cancerchronic inflammationestrogen receptorInterleukin-1progesterone receptor

Identifiers

PMID42450306
PMCPMC13362516

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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 OpenQuestion graph.