Evidence map›Paper›PMID 40901953›Full record

ArticleScience advances2025

HSF2 drives breast cancer progression by acting as a stage-specific switch between proliferation and invasion.

Jenny C Pessa, Oona Paavolainen, Hendrik S E Hästbacka, Mikael C Puustinen, Alejandro J Da Silva, Sandra Pihlström, Silvia Gramolelli, Pia Boström, Pauliina Hartiala, Emilia Peuhu and 2 more

Abstract read
In one paragraph

Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Adaptation to heat stress by diversification of the vertebrate heat shock transcription factor family.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
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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

12 authors.

Jenny C PessaFaculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland.ORCID 0000-0002-9113-6784
Oona PaavolainenTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.ORCID 0000-0003-1705-6310
Hendrik S E HästbackaFaculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland.ORCID 0000-0001-7793-1848
Mikael C PuustinenFaculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland.ORCID 0000-0002-1253-8532
Alejandro J Da SilvaFaculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland.ORCID 0000-0001-8116-555X
Sandra PihlströmFaculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland.ORCID 0000-0002-0505-9912
Silvia GramolelliFaculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland.
Pia BoströmUniversity of Turku and Turku University Hospital, Turku, Finland.ORCID 0000-0002-0611-3319
Pauliina HartialaDepartment of Plastic and General Surgery, Turku University Hospital, Turku, Finland.ORCID 0000-0002-7606-7813
Emilia PeuhuTurku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland.ORCID 0000-0003-4945-3046
Jenny JoutsenFaculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland.ORCID 0000-0002-7868-556X
Lea SistonenFaculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland.ORCID 0000-0003-1341-2867

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is hallmarked by phenotypic transitions enabling abnormal cell proliferation and invasion. The stress-protective transcription factor heat shock factor 2 (HSF2) is associated with cancer, but its function in breast carcinogenesis remains poorly understood. Analysis of human breast tumor samples and mouse in vivo xenografts uncovered that HSF2 expression and activity undergo dynamic changes as a function of tumor progression. HSF2 expression, nuclear localization, and coexpression with the proliferation marker Ki67 are increased in ductal carcinoma in situ (DCIS), suggesting that HSF2 designates hyperplastic cells underlying tumor expansion. In mouse xenografts, HSF2 localization switches from nuclear to cytoplasmic upon DCIS-to-invasive transition. Using cell-based models, we identify canonical transforming growth factor-β (TGF-β) signaling as the molecular mechanism regulating HSF2. TGF-β-mediated down-regulation of HSF2 allowed acquisition of an invasive cell phenotype, which was counteracted by ectopic HSF2. Together, we propose that HSF2 acts as a stage-specific switch between proliferation and invasion in breast cancer.

Indexed as

Breast NeoplasmsCarcinoma, Intraductal, NoninfiltratingHeat-Shock ProteinsTranscription FactorsAnimalsCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHeat Shock Transcription FactorsHumansMiceNeoplasm InvasivenessSignal TransductionTransforming Growth Factor betaHeat-Shock ProteinsHeat Shock Transcription FactorsHSF2 protein, humanTranscription FactorsTransforming Growth Factor beta

Identifiers

PMID40901953
PMCPMC12407055

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.