Evidence map›Paper›PMID 40569213›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Interfacial Stress Regulates Plasticity and Drug Resistance at the Breast Cancer-Host Interface.

Bram G Soliman, Peilin Tian, Jiuyu Cui, Kristopher A Kilian, J Justin Gooding

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

5 authors.

Bram G SolimanSchool of Chemistry, University of New South Wales, Sydney, New South Wales, 2052, Australia.ORCID https://orcid.org/0009-0003-7709-165X
Peilin TianSchool of Chemistry, University of New South Wales, Sydney, New South Wales, 2052, Australia.ORCID https://orcid.org/0009-0006-0339-6890
Jiuyu CuiSchool of Chemistry, University of New South Wales, Sydney, New South Wales, 2052, Australia.ORCID https://orcid.org/0009-0003-6404-4635
Kristopher A KilianSchool of Chemistry, University of New South Wales, Sydney, New South Wales, 2052, Australia.ORCID https://orcid.org/0000-0002-8963-9796
J Justin GoodingSchool of Chemistry, University of New South Wales, Sydney, New South Wales, 2052, Australia.ORCID https://orcid.org/0000-0002-5398-0597

Funding

National Cancer Institute of the National Institutes of Health R01CA251443National Health and Medical Research Council APP1185021National Health and Medical Research Council GNT1196648National Health and Medical Research Council GNT2019056NCI NIH HHS R01 CA251443
6 · The paper itself

Abstract

The confinement of breast cancer cells at the interface of the mammary gland lumen and its surrounding extracellular matrix is thought to be a key physical driver of cellular plasticity. The relationship between confinement-induced solid stress and drug resistance is not well understood due to a scarcity of models that faithfully isolate the contribution of confinement on cancer cell behavior. Herein, drop-on-demand printing is used to uniquely replicate the spatial compartmentalization of the native cancer-host interface: MCF-7 breast cancer cells are dispensed within bioinert cup-shaped alginate-based hydrogels in high-throughput to yield "confined" spheroids. Hydrogel confinement affects the emergence of CD44+-CD133+ cells at the spheroid interface that drives a two-fold increase in doxorubicin/tamoxifen resistance compared to control "unconfined" spheroids. Whilst the peripheral drug-resistant phenotype is observed clinically, the model is unique in facilitating the emergence of this population in an in vitro setting. Pharmacological modulation of mechanotransduction proteins (YAP, myosin), abrogated the emergence of this peripheral phenotype, implicating mechanotransduction pathways as an effective way to target solid stress-induced drug resistance. Together, this supports an "interfacial stress-stemness-drug resistance" relationship that sheds new light on the existing paradigm of spatial emergence of drug resistance in breast cancer.

Indexed as

Breast NeoplasmsCell PlasticityDrug Resistance, NeoplasmDoxorubicinFemaleHumansHydrogelsMCF-7 CellsMechanotransduction, CellularSpheroids, CellularTamoxifenDoxorubicinHydrogelsTamoxifencancercellular heterogeneityconfinementdrop‐on‐demand printingdrug deliverydrug resistancesolid stress

Identifiers

PMID40569213
PMCPMC12462989

What Socratic holds

Textmetadata
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 Socratic graph.