ArticleDisease models & mechanisms2023
Low HER2 expression in normal breast epithelium enables dedifferentiation and malignant transformation via chromatin opening.
Article in Disease models & mechanisms, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- In silico design of a multi-epitope vaccine against the triple negative breast cancer.Scientific reports · 2025Article
- Integrative proteo-genomic profiling uncovers key biomarkers of lapatinib resistance in HER2-positive breast cancer.British journal of cancer · 2025Article
- Characterisation of HER2-Driven Morphometric Signature in Breast Cancer and Prediction of Risk of Recurrence.Cancer medicine · 2025Article
- Combined SERS-Raman screening of HER2-overexpressing or silenced breast cancer cell lines.Journal of nanobiotechnology · 2024Article
- Pathological precision diagnosis and recent advances in HER2 low and ultralow in breast cancer: a narrative review.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2024Review
- Identification of mammalian transcription factors that bind to inaccessible chromatin.Nucleic acids research · 2023Article
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
Overexpression of the HER2 protein in breast cancer patients is a predictor of poor prognosis and resistance to therapies. We used an inducible breast cancer transformation system that allows investigation of early molecular changes. HER2 overexpression to similar levels as those observed in a subtype of HER2-positive breast cancer patients induced transformation of MCF10A cells and resulted in gross morphological changes, increased anchorage-independent growth of cells, and altered the transcriptional programme of genes associated with oncogenic transformation. Global phosphoproteomic analysis during HER2 induction predominantly detected an increase in protein phosphorylation. Intriguingly, this correlated with chromatin opening, as measured by ATAC-seq on acini isolated from 3D cell culture. HER2 overexpression resulted in opening of many distal regulatory regions and promoted reprogramming-associated heterogeneity. We found that a subset of cells acquired a dedifferentiated breast stem-like phenotype, making them likely candidates for malignant transformation. Our data show that this population of cells, which counterintuitively enriches for relatively low HER2 protein abundance and increased chromatin accessibility, possesses transformational drive, resulting in increased anchorage-independent growth in vitro compared to cells not displaying a stem-like phenotype.
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Registered trials
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.