The membrane-associated form of cyclin D1 enhances cellular invasion.

Autor: Chen K; Department of Cancer Biology, Thomas Jefferson University, Philadelphia, PA, 19107, USA., Jiao X; Pennsylvania Cancer and Regenerative Medicine Research Center, Baruch S. Blumberg Institute, Pennsylvania Biotechnology Center, Wynnewood, PA, 19096, USA., Ashton A; Pennsylvania Cancer and Regenerative Medicine Research Center, Baruch S. Blumberg Institute, Pennsylvania Biotechnology Center, Wynnewood, PA, 19096, USA., Di Rocco A; Pennsylvania Cancer and Regenerative Medicine Research Center, Baruch S. Blumberg Institute, Pennsylvania Biotechnology Center, Wynnewood, PA, 19096, USA., Pestell TG; Department of Cancer Biology, Thomas Jefferson University, Philadelphia, PA, 19107, USA., Sun Y; Department of Pathology, Medical College of Wisconsin, Milwaukee, WI, 53226, USA., Zhao J; Pennsylvania Cancer and Regenerative Medicine Research Center, Baruch S. Blumberg Institute, Pennsylvania Biotechnology Center, Wynnewood, PA, 19096, USA., Casimiro MC; Pennsylvania Cancer and Regenerative Medicine Research Center, Baruch S. Blumberg Institute, Pennsylvania Biotechnology Center, Wynnewood, PA, 19096, USA.; Dept of Science and Math, Abraham Baldwin Agricultural college, Tifton, GA, 31794, Georgia., Li Z; Pennsylvania Cancer and Regenerative Medicine Research Center, Baruch S. Blumberg Institute, Pennsylvania Biotechnology Center, Wynnewood, PA, 19096, USA., Lisanti MP; Biomedical Research Centre (BRC), Translational Medicine, School of Environment and Life Sciences, University of Salford, Manchester, United Kingdom., McCue PA; Department of Pathology, Anatomy and Cell Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, 19107, USA., Shen D; Departments of Biomedical Engineering, Washington University, St. Louis, MO, 63110, USA., Achilefu S; Departments of Biomedical Engineering, Washington University, St. Louis, MO, 63110, USA.; Departments of Radiology, Washington University, St. Louis, MO, 63110, USA.; Departments of Biochemistry & Molecular Biophysics, Washington University, St. Louis, MO, 63110, USA., Rui H; Department of Pathology, Medical College of Wisconsin, Milwaukee, WI, 53226, USA., Pestell RG; Pennsylvania Cancer and Regenerative Medicine Research Center, Baruch S. Blumberg Institute, Pennsylvania Biotechnology Center, Wynnewood, PA, 19096, USA. Richard.pestell@bblumberg.org.; The Wistar Cancer Center, Wistar Institute, Philadelphia, PA, 19104, USA. Richard.pestell@bblumberg.org.
Jazyk: angličtina
Zdroj: Oncogenesis [Oncogenesis] 2020 Sep 18; Vol. 9 (9), pp. 83. Date of Electronic Publication: 2020 Sep 18.
DOI: 10.1038/s41389-020-00266-y
Abstrakt: The essential G 1 -cyclin, CCND1, is a collaborative nuclear oncogene that is frequently overexpressed in cancer. D-type cyclins bind and activate CDK4 and CDK6 thereby contributing to G 1 -S cell-cycle progression. In addition to the nucleus, herein cyclin D1 was also located in the cytoplasmic membrane. In contrast with the nuclear-localized form of cyclin D1 (cyclin D1 NL ), the cytoplasmic membrane-localized form of cyclin D1 (cyclin D1 MEM ) induced transwell migration and the velocity of cellular migration. The cyclin D1 MEM was sufficient to induce G 1 -S cell-cycle progression, cellular proliferation, and colony formation. The cyclin D1 MEM was sufficient to induce phosphorylation of the serine threonine kinase Akt (Ser473) and augmented extranuclear localized 17β-estradiol dendrimer conjugate (EDC)-mediated phosphorylation of Akt (Ser473). These studies suggest distinct subcellular compartments of cell cycle proteins may convey distinct functions.
Databáze: MEDLINE
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