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SHR Neuro Cancer Cardio Lipid Metab Microb

Pozo, K; Castro-Rivera, E; Tan, C; Plattner, F; Schwach, G; Siegl, V; Meyer, D; Guo, A; Gundara, J; Mettlach, G; Richer, E; Guevara, JA; Ning, L; Gupta, A; Hao, G; Tsai, LH; Sun, X; Antich, P; Sidhu, S; Robinson, BG; Chen, H; Nwariaku, FE; Pfragner, R; Richardson, JA; Bibb, JA.
The role of Cdk5 in neuroendocrine thyroid cancer.
Cancer Cell. 2013; 24(4):499-511 Doi: 10.1016/j.ccr.2013.08.027 [OPEN ACCESS]
Web of Science PubMed FullText FullText_MUG

Co-authors Med Uni Graz: Pfragner Roswitha; Schwach Gert; Siegl Veronika
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Abstract:: Medullary thyroid carcinoma (MTC) is a neuroendocrine cancer that originates from calcitonin-secreting parafollicular cells, or C cells. We found that Cdk5 and its cofactors p35 and p25 are highly expressed in human MTC and that Cdk5 activity promotes MTC proliferation. A conditional MTC mouse model was generated and corroborated the role of aberrant Cdk5 activation in MTC. C cell-specific overexpression of p25 caused rapid C cell hyperplasia leading to lethal MTC, which was arrested by repressing p25 overexpression. A comparative phosphoproteomic screen between proliferating and arrested MTC identified the retinoblastoma protein (Rb) as a crucial Cdk5 downstream target. Prevention of Rb phosphorylation at Ser807/Ser811 attenuated MTC proliferation. These findings implicate Cdk5 signaling via Rb as critical to MTC tumorigenesis and progression.
Find related publications in this database (using NLM MeSH Indexing): Animals -; Carcinoma, Medullary - metabolism; Carcinoma, Neuroendocrine - metabolism; Cell Line, Tumor -; Cell Proliferation -; Cell Survival -; Cyclin-Dependent Kinase 5 - metabolism; Disease Progression -; Gene Expression Regulation, Neoplastic -; Humans -; Mice -; Mice, Transgenic -; Phosphorylation -; Retinoblastoma Protein - metabolism; Signal Transduction -; Thyroid Neoplasms - metabolism; Time Factors -; Transgenes -