ArticlePLoS genetics2012
EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors in transgenic mice.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.
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Who cites it
124 citing papers in PubMed, 197 citations in OpenAlex.
- CK8/18 and Claudin Profile of Female Breast Cancers from Botswana.Breast cancer : basic and clinical research · 2026Article
- The Role of Mesenchymal Stem Cells in Drug Resistance in Lung Neoplasms.Journal of cancer prevention · 2025Review
- Advancing In Vitro Tools for Oncologic Research in Cats and Dogs.Veterinary sciences · 2025Review
- The inflammasome sensor NLRP3 interacts with REV7 to maintain genome integrity through homologous recombination.Nucleic acids research · 2025Article
- Specific modulation of 28S_Um2402 rRNA 2'-NAR cancer · 2025Article
- EMT-driven plasticity prospectively increases cell-cell variability to promote therapeutic adaptation in breast cancer.Cancer cell international · 2025Article
- Intricate ribosome composition and translational reprogramming in epithelial-mesenchymal transition.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The molecular features of lung cancer stem cells in dedifferentiation process-driven epigenetic alterations.The Journal of biological chemistry · 2024Review
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- Cooperative pro-tumorigenic adaptation to oncogenic RAS through epithelial-to-mesenchymal plasticity.Science advances · 2024Article
- βCells · 2024Article
- Update on Epithelial-Mesenchymal Plasticity in Cancer Progression.Annual review of pathology · 2024Review
- Stromal heterogeneity may explain increased incidence of metaplastic breast cancer in women of African descent.Nature communications · 2023Article
- FAP, CD10, and GPR77-labeled CAFs cause neoadjuvant chemotherapy resistance by inducing EMT and CSC in gastric cancer.BMC cancer · 2023Article
- FRA-1 as a Regulator of EMT and Metastasis in Breast Cancer.International journal of molecular sciences · 2023Review
- PLAC8 contributes to the malignant behaviors of cervical cancer cells by activating the SOX4-mediated AKT pathway.Histochemistry and cell biology · 2023Article
- Intestinal Epithelial Cells Adapt to Chronic Inflammation through Partial Genetic Reprogramming.Cancers · 2023Article
- Research progress of Claudin-low breast cancer.Frontiers in oncology · 2023Review
- Article
64 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial-mesenchymal transition (EMT) is an embryonic transdifferentiation process consisting of conversion of polarized epithelial cells to motile mesenchymal ones. EMT-inducing transcription factors are aberrantly expressed in multiple tumor types and are known to favor the metastatic dissemination process. Supporting oncogenic activity within primary lesions, the TWIST and ZEB proteins can prevent cells from undergoing oncogene-induced senescence and apoptosis by abolishing both p53- and RB-dependent pathways. Here we show that they also downregulate PP2A phosphatase activity and efficiently cooperate with an oncogenic version of H-RAS in malignant transformation of human mammary epithelial cells. Thus, by down-regulating crucial tumor suppressor functions, EMT inducers make cells particularly prone to malignant conversion. Importantly, by analyzing transformed cells generated in vitro and by characterizing novel transgenic mouse models, we further demonstrate that cooperation between an EMT inducer and an active form of RAS is sufficient to trigger transformation of mammary epithelial cells into malignant cells exhibiting all the characteristic features of claudin-low tumors, including low expression of tight and adherens junction genes, EMT traits, and stem cell-like characteristics. Claudin-low tumors are believed to be the most primitive breast malignancies, having arisen through transformation of an early epithelial precursor with inherent stemness properties and metaplastic features. Challenging this prevailing view, we propose that these aggressive tumors arise from cells committed to luminal differentiation, through a process driven by EMT inducers and combining malignant transformation and transdifferentiation.
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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.