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Lisa Wimmer

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    EP1.03 - Biology (ID 193)

    • Event: WCLC 2019
    • Type: E-Poster Viewing in the Exhibit Hall
    • Track: Biology
    • Presentations: 1
    • Now Available
    • Moderators:
    • Coordinates: 9/08/2019, 08:00 - 18:00, Exhibit Hall
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      EP1.03-31 - Cell Migration and Epithelial Mesenchymal Transition in Lung Cancer - Different Roads and Common Themes (Now Available) (ID 930)

      08:00 - 18:00  |  Author(s): Lisa Wimmer

      • Abstract
      • Slides


      Cell migration is an indispensable function for many cells in multicellular organisms. When deregulated, however, especially in conjunction with the ability to degrade extracellular matrix and invade surrounding tissues, it is a hallmark of malignancy and forms the basis for cancer metastasis. This is often linked to epithelial mesenchymal transition (EMT) which is widely recognized in cancer cell biology to be intricately connected to metastasis, drug resistance and stemness. Multiple extracellular stimuli that induce EMT and cell migration in diverse cellular contexts have been described, nevertheless, a lot still needs to be learned about pathway-specific mechanisms. We have chosen the Ras-mutated A549 lung adenocarcinoma cell line for investigating how the two growth factors EGF and TGFb, which each play fundamental roles in tumor development but activate clearly distinct signaling cascades both stimulate EMT and migration individually and when acting in cooperation.


      A549 cells were treated with EGF, TGFb or a combination of both in serum-free conditions. Also, inhibitors of downstream pathways were used at sub-lethal concentrations. Changes in cell morphology were determined using ImageJ from microscopy images. Cell migration was assessed by live cell videomicroscopy followed by singe cell tracking. The invasive capacity was determined by a 3D sprouting assay. Expression changes were identified by qPCR and immunoblots.


      Treatment with TGFb and EGF resulted in cell scattering and distinct changes in cell morphology, which were different for each growth factor. While cells treated with TGFb showed classic EMT-like, elongated morphology, cells exposed to EGF rounded up. Combining both factors resulted in a mixed population. EGF-induced changes could be prevented by Akt but not MAPK inhibitors. Importantly, each growth factor induced a significant increase in cell migration compared to untreated cells and the combination of both factors stimulated migration even further. Interestingly, the increase in migration occurred earlier with EGF than with TGFb, and this was in concordance with increased pERK levels. However, only TGFb was able to induce significantly increased sprouting.


      Our data describes two independent signaling pathways which both are able to induce cell scattering and cell migration, albeit along different roads. Especially in cancer cells, a better understanding of signaling pathway-dependency of EMT and migration and potential cross talks could lead to more effective antimetastatic therapies.

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