ArticlePloS one2014
Highly adaptable triple-negative breast cancer cells as a functional model for testing anticancer agents.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- A phenotype-based cell culture model of melanoma cells that persist as residual disease after therapies leading to recurrence.Research square · 2026Article
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- Sensitization of Resistant Breast Cancer Cells with a Jumonji Family Histone Demethylase Inhibitor.Cancers · 2022Article
- A mechanistic modeling framework reveals the key principles underlying tumor metabolism.PLoS computational biology · 2022Article
- Inhibition of resistant triple-negative breast cancer cells with low-dose 6-mercaptopurine and 5-azacitidine.Oncotarget · 2021Article
- Stapled EGFR peptide reduces inflammatory breast cancer and inhibits additional HER-driven models of cancer.Journal of translational medicine · 2019Article
- Evaluation of 6-mercaptopurine in a cell culture model of adaptable triple-negative breast cancer with metastatic potential.Oncotarget · 2019Article
- A usable model of "decathlon winner" cancer cells in triple-negative breast cancer: survival of resistant cancer cells in quiescence.Oncotarget · 2018Article
- Roles of Grainyhead-like transcription factors in cancer.Oncogene · 2017Review
- Near-simultaneous intravital microscopy of glucose uptake and mitochondrial membrane potential, key endpoints that reflect major metabolic axes in cancer.Scientific reports · 2017Article
- GRHL2 suppresses tumor metastasis via regulation of transcriptional activity of RhoG in non-small cell lung cancer.American journal of translational research · 2017Article
- Grainyhead-like 2 Reverses the Metabolic Changes Induced by the Oncogenic Epithelial-Mesenchymal Transition: Effects on Anoikis.Molecular cancer research : MCR · 2016Article
- Article
- Milk: an epigenetic amplifier of FTO-mediated transcription? Implications for Western diseases.Journal of translational medicine · 2015Review
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Authors and funding
7 authors.
Funding
Abstract
A major obstacle in developing effective therapies against solid tumors stems from an inability to adequately model the rare subpopulation of panresistant cancer cells that may often drive the disease. We describe a strategy for optimally modeling highly abnormal and highly adaptable human triple-negative breast cancer cells, and evaluating therapies for their ability to eradicate such cells. To overcome the shortcomings often associated with cell culture models, we incorporated several features in our model including a selection of highly adaptable cancer cells based on their ability to survive a metabolic challenge. We have previously shown that metabolically adaptable cancer cells efficiently metastasize to multiple organs in nude mice. Here we show that the cancer cells modeled in our system feature an embryo-like gene expression and amplification of the fat mass and obesity associated gene FTO. We also provide evidence of upregulation of ZEB1 and downregulation of GRHL2 indicating increased epithelial to mesenchymal transition in metabolically adaptable cancer cells. Our results obtained with a variety of anticancer agents support the validity of the model of realistic panresistance and suggest that it could be used for developing anticancer agents that would overcome panresistance.
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