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Y. Gorzalczany

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    Poster Display session (Friday) (ID 65)

    • Event: ELCC 2018
    • Type: Poster Display session
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 4/13/2018, 12:30 - 13:00, Hall 1
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      10P - The micro-environmental cross talk between mast cells and lung cancer cells through cell-to-cell contact (ID 170)

      12:30 - 13:00  |  Author(s): Y. Gorzalczany

      • Abstract
      • Slides

      Mast cells (MCs) are key effectors in allergic reactions, but are also involved in tissue remodeling, wound healing and protection against pathogens. MCs infiltrate tumors and their number within the tumor microenvironment in certain cancer types, such as lung cancer, has been correlated with poor prognosis. The nature of crosstalk between lung cancer and MCs remains poorly resolved. In this study, we investigated the activation patterns within the MCs following cell-to-cell contact with lung cancer cells.

      Human MCs (HMC-1 and LAD-2) were exposed to Human lung cancer cell (H1299) derived membranes to recapitulate cell contact mediated activation. Lysates of MCs were tested for protein expression and posttranslational modifications (i.e. phosphorylation) by targeted western blotting. We unraveled the intracellular signaling molecules that are necessary for this signaling pathway by a pharmacological approach using several inhibitors. Each treatment was repeated at least 3 times.

      H1299 membrane exposure activated the ERK1/2 MAP kinases in HMC-1 and in LAD-2 cells. AKT signaling was also activated in LAD-2 cells as a result of this contact. Furthermore, we discovered that inhibition of protein kinase C (PKC) augments the activation of ERK1/2 in LAD-2 cells, while it inhibits ERK1/2 activation in HMC-1 cells. Activation of AKT is inhibited by PI3K and PKC inhibitors.

      Our results suggest that H1299 membranes activate ERK1/2 in MCs. In addition, we discovered that there is an important difference between ERK1/2 MAP kinase signal transduction in HMC-1 and LAD-2 cells, whereby PKC is an inhibitor of the H1299 stimulated activation of ERK1/2 in LAD-2 cells, while it mediates ERK 1/2 activation in HMC-1 cells. Furthermore, we can conclude that H1299 membranes activate AKT and that the activation is mediated by PI3K and PKC. Rachel Shemesh and Yaara Gorzalczany contributed equally to this work. Correspondence Authors: Nir Peled, Ronit Sagi-Eisenberg.

      Clinical trial identification:

      Legal entity responsible for the study:
      Prof. Nir Peled, Prof. Ronit Sagi-Eisenberg

      Has not received any funding

      All authors have declared no conflicts of interest.

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