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Activation of PKA leads to mesenchymal-to-epithelial transition and loss of tumor-initiating ability
Open accessAbstract
Have cancer stem cells MET their match?: Solid tumors have been hypothesized to contain a subset of highly aggressive cells that fuel tumor growth and metastasis. The search is on for drugs that selectively kill or diminish the malignant properties of these tumor-initiating cells (TICs; previously called “cancer stem cells”). Pattabiraman et al. hypothesized that compounds that induce TICs to undergo a phenotypic change called the mesenchymal-to-epithelial transition (MET) would therefore cause TICs to lose their tumor-initiating ability. Indeed, drugs activating the protein kinase A signaling pathway triggered an epigenetic reprogramming of TICs that resulted in the cells acquiring a more benign epithelial-like phenotype. Science , this issue p. 10.1126/science.aad3680
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Metadata
- Authors
- Pattabiraman, D. R., Bierie, B., Kober, K. I., Thiru, P., Krall, J. A., Zill, C., Reinhardt, F., Tam, W. L., & Weinberg, R. A.
- Affiliations
- Whitehead Institute for Biomedical Research (US)
- Corresponding author
- Weinberg, Robert A.
- ORCID
- Venue
- Science
- Published
- 2016-03-04
- Volume
- 351
- Issue
- 6277
- Pages
- aad3680-aad3680
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC5131720
- OpenAlex
- W2289283229
- Cited by
- 332
- References
- 60
- Citations by year
- 2026: 13 · 2025: 15 · 2024: 32 · 2023: 26 · 2022: 35 · 2021: 36 · 2020: 47 · 2019: 32 · 2018: 36 · 2017: 41 · 2016: 18
- FWCI
- 22.81
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc-sa)
- PMC
- Funders
- National Health and Medical Research Council of Australia (NHMRC APP1071853)
- National Research Foundation, Singapore (NRF-NRFF2015-04)
- National Medical Research Council, Singapore (NMRC/TCR/007-NCC/2013)
- Ludwig Center for Molecular Oncology at MIT
- Breast Cancer Research Foundation
- Samuel Waxman Cancer Research Foundation
- NIH (R01-CA078461)
- American Cancer Society
- D. K. Ludwig Foundation Cancer Research
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- protein kinase A, mesenchymal-epithelial transition, cancer stem cells, PHF2, histone demethylase, epigenetic reprogramming, cAMP signaling, mammary epithelial cells, differentiation therapy
- MeSH terms
- Adenosine Monophosphate, Animals, Breast Neoplasms, Cell Transformation, Neoplastic, Cholera Toxin, Enzyme Activation, Epithelial Cells, Female, Colforsin, Humans, Mesoderm, Neoplastic Stem Cells, Second Messenger Systems, Cyclic AMP-Dependent Protein Kinases, Homeodomain Proteins, Xenograft Model Antitumor Assays, Mammary Glands, Human, Epigenesis, Genetic, Cell Line, Tumor, Mice, Histone Demethylases, Epithelial-Mesenchymal Transition
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