Coronin-1C (CRN2, coronin-3) dependent migration and invasion of tumor cells

Research focus

Dynamic reorganization of the actin cytoskeleton is required for many physiological processes like leading edge protrusion, cell locomotion and cytokinesis. It is achieved by a variety of proteins including the coronins. Coronins are conserved actin-binding proteins that promote processes relying on a remodelling of the actin cytoskeleton. We study the ubiquitously expressed CRN2 (synonyms:
coronin-1C, coronin-3). It localizes to the cytosol and to lamellipodia and membrane ruffles in fibroblasts and HEK293 cells and directly binds to and bundles F-actin. Overexpression and knockdown studies indicate that CRN2 is required for the formation of lamellipodia and affects wound healing, cell migration and invasion into extracellular matrix. Analysis of human brain tumors showed that CRN2 is associated with the malignant phenotype of diffuse gliomas. Goal of our project is to define the contribution of CRN2 to tumor malignancy, to analyse the molecular mechanisms of CRN2 in tumor cell formation and metastasis and to determine CRN2 expression as a factor for prognosis. We will establish a mouse model, study the mechanism and regulation of CRN2 interaction with the actin cytoskeleton, identify further interactions of CRN2 and elucidate how these features contribute to the role of CRN2 in cancer progression.

Coronin-1C (CRN2, coronin-3) abhängige bewegung und Invasion von Tumorzellen

Coronin2 (CRN2) ist ein ubiquitär exprimiertes F-Aktin bindendes Protein mit Funktionen in der in vitro Wundheilung, Zellbewegung und Invasion in die Extrazellularmatrix. In menschlichen Gehirntumoren ist die CRN2 Expression mit dem malignen Phänotyp diffuser Gliome assoziiert. Ziel dieses Projekts ist die Analyse der Rolle von CRN2 für die Tumorbildung und Tumorprogression wie auch die Analyse der zugrundeliegenden molekularen Mechanismen. Dazu werden wir Mausmodelle für in vivo Studien etablieren sowie in biochemischen und zellbiologischen Untersuchungen die Funktion von CRN2 in der Regulation der Zytoskelettdynamik untersuchen, Bindepartner identifizieren und klären, welche Bedeutung diese Faktoren für die Tumorprogression besitzen.

Principal Investigators

Angelika Noegel

Prof. Dr. Angelika A. Noegel

Institute of Biochemistry I
Medical Faculty
University of Cologne
Josef-Stelzmann-Str. 52
50931 Cologne
Phone: +49-(0)221-478 6980
Fax: +49-(0)221-478 6979
Email:

Scientific career

1971-1976
University of Würzburg (Biology)
1979
PhD, Institute of Microbiology, University of Würzburg (Prof. Dr. W. Goebel)
1979-1983
Research associate, Laboratory of Bacteriology and Immunology, The Rockefeller University, New York (Prof. Dr. E. C. Gotschlich)
1983-1997
Research associate and group leader, Max-Planck-Institute for Biochemistry, Martinsried, FRG
1997
C4-Professor, Institute of Biochemistry I, Medical Faculty, University of Cologne
Christoph Clemen

PD Dr. Christoph S. Clemen

Institute of Biochemistry I
Medical Faculty
University of Cologne
Josef-Stelzmann-Str. 52
50931 Cologne
Phone: +49-(0)221-478 6980
Fax: +49-(0)221-478 6979
Email:

Scientific career

1995-2001
University of Cologne (Human Medicine)
2002
Dr. med., Institute of Biochemistry I, Medical Faculty, University of Cologne (Prof. Dr. A. A. Noegel)
2003
Research associate and group leader, Institute of Biochemistry I, Medical Faculty, University of Cologne
2007
Medical specialist for Biochemistry
2007
‘Habilitation’ in Biochemistry and Molecular Biology

PhD Students

Anja Ziemann

News

09 May 2012
CRC832 Seminar Series

Transcriptional networks regulating EMT and tumor progression (G. Christofori)
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14 - 16 May 2012
International Symposium of the Collaborative Research Center 832
Bad Neuenahr, Germany
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27 Feb 2012
Gunther Hartmann receives the Leibniz Prize 2012 together with Christian Kurts
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Gender & Family Support
Flyer: women in science | work-life-balance »

Publications
aPKC phosphorylates JAM-A at Ser285 to promote cell contact maturation and tight junction formation (Iden S et al.)
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