Cell Migration Group

We are investigating the role ion channels and ion transporters play in tumor and immune cell migration. In particular, we focus on Ca2+ sensitive K+ channels, TRP channels, and the Na+/H+ exchanger. The key question addressed by our research is: Why are these ion transport proteins required for cell migration? To this end we apply predominantly imaging techniques such as time-lapse videomicroscopy, live-cell fluorescence microscopy, TIRF microscopy and ionic imaging and atomic force microscopy.

The group is supported by the expert technical assistance of Ilka Neumann, Sarah Sargin and Sandra Schimmelpfennig.

 

  • 1. Function of transport proteins in pancreatic stellate cells

    A. Schwab

    V. Hofschröer

    T. Loeck

    This project is pursued within the framework of the European Marie Skłodowska Curie Innovative Training Network "pHioniC". It was originally initiated within the "IonTraC" network (2011-15) that was built around the study of ion transport proteins in pancreatic ductal adenocarcinoma (PDAC). We are studying how the crosstalk between ion channels and transporters in pancreatic stellate cells and the PDAC microenvironment drives the progression of the disease.

     

     

     

     

     

     

     

     

     

     

     

     

     

     

     

     

     

     

     

     

     

    pHioniC  

    pH and Ion Transport in Pancreatic Cancer – pHioniC

    pHioniC is a Marie Skłodowska Curie Innovative Training Network on the role of pH and ion transport proteins in pancreatic cancer. It is funded by the European Commission from 1st November, 2018 to 31th October, 2022.

  • 2. Ion channels in neutrophil function

    Neutrophil activation comprises multiple functions such as extravasation, chemotaxis, ROS production or phagocytosis. It is usually initiated by the binding of  chemokines and chemoattractants to their G-protein coupled receptors (GPCRs). Dysfunction of any of the neutrophil defense mechanism may have serious consequences - from prolonged infection to autoimmune diseases.
    TRPM2 is a Na+ and Ca2+-permeable channel expressed in neutrophils. The function of neutrophils lacking TRPM2 channels is disturbed, but the causes are not yet fully understood. Here we analyze TRPM2 mechanism of action and its role in neutrophil chemotaxis and ion homeostasis.

                                 K. Najder

  • 3. KCa3.1 channels in the progression of non-small cell lung cancer (NSCLC)

    This project builds upon mounting evidence that ion channels underlie many of the hallmarks of cancer. They are expressed aberrantly in cancer and are central players in proliferation, apoptosis, angiogenesis, cell-matrix interaction and migration/invasion. Here, we want to address the question whether KCa3.1 channels contribute to the development of an invasive, metastatic phenotype of NSCLC cells and thereby promote the progression of the disease.                                                                                                                                                                

                                                                                                                                 

                                                                                                                     E.Bulk

     

     

     

     

     

     

                                                                                                                    L.Todesca

     

     

  • 4. Mechano-signaling in pancreatic stellate cells

    Z. Pethö
    M. Rugi

    In the healthy pancreas, pancreatic stellate cells (PSCs) are enveloped in a soft meshwork of extracellular matrix, mainly next to acinar or ductal cells. In chronic pancreatitis and pancratic cancer, the environment of these cells changes dramatically to a stiff, fibrous tissue, which provokes functional changes in PSCs. The exact nature of these changes is yet unknown and thus we aim to elucidate the key sensors of mechanical stress in PSCs and what cellular reactions they initiate.       

    1. Fels B et al., Eur Biophys J. 2016