Cited by 332Cancer Cells and MetastasisTGF-β signaling in diseasesEpigenetics and DNA Methylation

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Activation of PKA leads to mesenchymal-to-epithelial transition and loss of tumor-initiating ability

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Pattabiraman, Diwakar R., Bierie, Brian, Kober, Katharina Isabelle, Thiru, Prathapan, Krall, Jordan A., Zill, Christina, Reinhardt, Ferenc, Tam, Wai Leong, Weinberg, Robert A.·2016·Science

DOI 10.1126/science.aad3680PMC PMC5131720

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Abstract

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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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: Pattabiraman, Diwakar R.
Kober, Katharina Isabelle
Thiru, Prathapan
Krall, Jordan A.
Tam, Wai Leong
Weinberg, Robert A.
Venue: Science
Publisher: American Association for the Advancement of Science (AAAS)
Published: 2016-03-04
Volume: 351
Issue: 6277
Pages: aad3680-aad3680
ISSN: 0036-8075 (ISSN-L)
1095-9203
DOI: 10.1126/science.aad3680
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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Activation of PKA leads to mesenchymal-to-epithelial transition and loss of tumor-initiating ability

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