ArticlePloS one2013
Genomic insights into triple-negative and HER2-positive breast cancers using isogenic model systems.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 13 citations in OpenAlex.
- Estrogen receptor alpha dynamics and plasticity during endocrine resistance.Biology direct · 2025Article
- Analysis of methylation features associated with neoadjuvant efficacy in HER2-positive breast cancer.Frontiers in oncology · 2025Article
- Transcriptome profiling of the interconnection of pathways involved in malignant transformation and response to hypoxia.Oncotarget · 2018Article
- Chromosome 19 miRNA cluster and CEBPB expression specifically mark and potentially drive triple negative breast cancers.PloS one · 2018Article
- Rhus coriaria suppresses angiogenesis, metastasis and tumor growth of breast cancer through inhibition of STAT3, NFκB and nitric oxide pathways.Scientific reports · 2016Article
- Pharmacological induction of cell surface GRP78 contributes to apoptosis in triple negative breast cancer cells.Oncotarget · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionIn general, genomic signatures of breast cancer subtypes have little or no overlap owing to the heterogeneous genetic backgrounds of study samples. Thus, obtaining a reliable signature in the context of isogenic nature of the cells has been challenging and the precise contribution of isogenic triple negative breast cancer (TNBC) versus non-TNBC remains poorly defined.
methodsWe established isogenic stable cell lines representing TNBC and Human Epidermal Growth Factor Receptor 2 positive (HER2+) breast cancers by introducing HER2 in TNBC cell lines MDA-MB-231 and MDA-MB-468. We examined protein level expression and functionality of the transfected receptor by treatment with an antagonist of HER2. Using microarray profiling, we obtained a comprehensive gene list of differentially expressed between TNBC and HER2+ clones. We identified and validated underlying isogenic components using qPCR and also compared results with expression data from patients with similar breast cancer subtypes.
resultsWe identified 544 and 1087 statistically significant differentially expressed genes between isogenic TNBC and HER2+ samples in MDA-MB-231 and MDA-MB-468 backgrounds respectively and a shared signature of 49 genes. By comparing results from MDA-MB-231 and MDA-MB-468 backgrounds with two patient microarray datasets, we identified 17 and 22 common genes with same expression trend respectively. Additionally, we identified 56 and 78 genes from MDA-MB-231 and MDA-MB-468 comparisons respectively present in our published RNA-seq data.
conclusionsUsing our unique model system, we have identified an isogenic gene expression signature between TNBC and HER2+ breast cancer. A portion of our results was also verified in patient data samples, indicating an existence of isogenic element associated with HER2 status between genetically heterogeneous breast cancer samples. These findings may potentially contribute to the development of molecular platform that would be valuable for diagnostic and therapeutic decision for TNBC and in distinguishing it from HER2+ subtype.
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