Citation

  • Authors: Steed, E., Elbediwy, A., Vacca, B., Dupasquier, S., Hemkemeyer, S. A., Suddason, T., Costa, A. C., Beaudry, J. B., Zihni, C., Gallagher, E., Pierreux, C. E., Balda, M. S., Matter, K.
  • Year: 2014
  • Journal: J Cell Biol 204 821-38
  • Applications: in vitro / DNA, siRNA / INTERFERin, jetPEI
  • Cell types:
    1. Name: Caco-2
      Description: Human colon carcinoma epithelial cells
    2. Name: MIA PaCa-2
      Description: Human pancreatic cells
      Known as: MIAPaCa-2

Abstract

MarvelD3 is a transmembrane component of tight junctions, but there is little evidence for a direct involvement in the junctional permeability barrier. Tight junctions also regulate signaling mechanisms that guide cell proliferation; however, the transmembrane components that link the junction to such signaling pathways are not well understood. In this paper, we show that MarvelD3 is a dynamic junctional regulator of the MEKK1-c-Jun NH2-terminal kinase (JNK) pathway. Loss of MarvelD3 expression in differentiating Caco-2 cells resulted in increased cell migration and proliferation, whereas reexpression in a metastatic tumor cell line inhibited migration, proliferation, and in vivo tumor formation. Expression levels of MarvelD3 inversely correlated with JNK activity, as MarvelD3 recruited MEKK1 to junctions, leading to down-regulation of JNK phosphorylation and inhibition of JNK-regulated transcriptional mechanisms. Interplay between MarvelD3 internalization and JNK activation tuned activation of MEKK1 during osmotic stress, leading to junction dissociation and cell death in MarvelD3-depleted cells. MarvelD3 thus couples tight junctions to the MEKK1-JNK pathway to regulate cell behavior and survival.

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