ArticleCancer research2008
Targeted deletion of Prkar1a reveals a role for protein kinase A in mesenchymal-to-epithelial transition.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Stress Biology in Cancer: Neuroendocrine-Immune Mechanisms Linking Tumor Progression to Translational Interventions.Cancer communications (London, England) · 2026Review
- Epithelial elements in superficial angiomyxomas: mimicry of adnexal development, and mesenchymal-to-epithelial transition.Histopathology · 2025Article
- Adrenocortical Carcinomas: Molecular Pathogenesis, Treatment Options, and Emerging Immunotherapy and Targeted Therapy Approaches.The oncologist · 2024Review
- Dualistic Effects of PRKAR1A as a Potential Anticancer Target in Cancer Cells and Cancer-Derived Stem Cells.International journal of molecular sciences · 2024Article
- Chronic Stress: Impacts on Tumor Microenvironment and Implications for Anti-Cancer Treatments.Frontiers in cell and developmental biology · 2021Review
- Limiting Self-Renewal of the Basal Compartment by PKA Activation Induces Differentiation and Alters the Evolution of Mammary Tumors.Developmental cell · 2020Article
- Tumor mutation burden and recurrent tumors in hereditary lung cancer.Cancer medicine · 2019Article
- The AFrontiers in pharmacology · 2018Article
- Dibutyryl-cAMP attenuates pulmonary fibrosis by blocking myofibroblast differentiation via PKA/CREB/CBP signaling in rats with silicosis.Respiratory research · 2017Article
- A siRNA screen reveals the prosurvival effect of protein kinase A activation in conditions of unresolved endoplasmic reticulum stress.Cell death and differentiation · 2016Article
- Growth hormone and risk for cardiac tumors in Carney complex.Endocrine-related cancer · 2016Article
- Harnessing protein kinase A activation to induce mesenchymal-epithelial programs to eliminate chemoresistant, tumor-initiating breast cancer cells.Translational cancer research · 2016Article
- Activation of PKA leads to mesenchymal-to-epithelial transition and loss of tumor-initiating ability.Science (New York, N.Y.) · 2016Article
- PKA signaling drives mammary tumorigenesis through Src.Oncogene · 2015Article
- Loss of Prkar1a leads to Bcl-2 family protein induction and cachexia in mice.Cell death and differentiation · 2014Article
- CREB-binding protein (CBP) regulates β-adrenoceptor (β-AR)-mediated apoptosis.Cell death and differentiation · 2013Article
- Thyroid-specific ablation of the Carney complex gene, PRKAR1A, results in hyperthyroidism and follicular thyroid cancer.Endocrine-related cancer · 2012Article
- Association between E-cadherin (CDH1) polymorphisms and papillary thyroid carcinoma risk in Han Chinese population.Endocrine · 2012Article
- Differential role of PKA catalytic subunits in mediating phenotypes caused by knockout of the Carney complex gene Prkar1a.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Alternate protein kinase A activity identifies a unique population of stromal cells in adult bone.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Dysregulation of protein kinase A (PKA) activity, caused by loss of function mutations in PRKAR1A, is known to induce tumor formation in the inherited tumor syndrome Carney complex (CNC) and is also associated with sporadic tumors of the thyroid and adrenal. We have previously shown that Prkar1a(+/-) mice develop schwannomas reminiscent of those seen in CNC and that similar tumors are observed in tissue-specific knockouts (KO) of Prkar1a targeted to the neural crest. Within these tumors, we have previously described the presence of epithelial islands, although the nature of these structures was unclear. In this article, we report that these epithelial structures are derived from KO cells originating in the neural crest. Analysis of the mesenchymal marker vimentin revealed that this protein was markedly down-regulated not only from the epithelial islands, but also from the tumor as a whole, consistent with mesenchymal-to-epithelial transition (MET). In vitro, Prkar1a null primary mouse embryonic fibroblasts, which display constitutive PKA signaling, also showed evidence for MET, with a loss of vimentin and up-regulation of the epithelial marker E-cadherin. Reduction of vimentin protein occurred at the posttranslational level and was rescued by proteasomal inhibition. Finally, this down-regulation of vimentin was recapitulated in the adrenal nodules of CNC patients, confirming an unexpected and previously unrecognized role for PKA in MET.
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