TY - JOUR
T1 - Identification of a novel anoikis signalling pathway using the fungal virulence factor gliotoxin
AU - Haun, Florian
AU - Neumann, Simon
AU - Peintner, Lukas
AU - Wieland, Katrin
AU - Habicht, Jüri
AU - Schwan, Carsten
AU - Østevold, Kristine
AU - Koczorowska, Maria Magdalena
AU - Biniossek, Martin
AU - Kist, Matthias
AU - Busch, Hauke
AU - Boerries, Melanie
AU - Davis, Roger J.
AU - Maurer, Ulrich
AU - Schilling, Oliver
AU - Aktories, Klaus
AU - Borner, Christoph
PY - 2018/12/1
Y1 - 2018/12/1
N2 - Anoikis is a form of apoptosis induced by cell detachment. Integrin inactivation plays a major role in the process but the exact signalling pathway is ill-defined. Here we identify an anoikis pathway using gliotoxin (GT), a virulence factor of the fungus Aspergillus fumigatus, which causes invasive aspergillosis in humans. GT prevents integrin binding to RGD-containing extracellular matrix components by covalently modifying cysteines in the binding pocket. As a consequence, focal adhesion kinase (FAK) is inhibited resulting in dephosphorylation of p190RhoGAP, allowing activation of RhoA. Sequential activation of ROCK, MKK4/MKK7 and JNK then triggers pro-apoptotic phosphorylation of Bim. Cells in suspension or lacking integrin surface expression are insensitive to GT but are sensitised to ROCK-MKK4/MKK7-JNK-dependent anoikis upon attachment to fibronectin or integrin upregulation. The same signalling pathway is triggered by FAK inhibition or inhibiting integrin αV/β3 with Cilengitide. Thus, GT can target integrins to induce anoikis on lung epithelial cells.
AB - Anoikis is a form of apoptosis induced by cell detachment. Integrin inactivation plays a major role in the process but the exact signalling pathway is ill-defined. Here we identify an anoikis pathway using gliotoxin (GT), a virulence factor of the fungus Aspergillus fumigatus, which causes invasive aspergillosis in humans. GT prevents integrin binding to RGD-containing extracellular matrix components by covalently modifying cysteines in the binding pocket. As a consequence, focal adhesion kinase (FAK) is inhibited resulting in dephosphorylation of p190RhoGAP, allowing activation of RhoA. Sequential activation of ROCK, MKK4/MKK7 and JNK then triggers pro-apoptotic phosphorylation of Bim. Cells in suspension or lacking integrin surface expression are insensitive to GT but are sensitised to ROCK-MKK4/MKK7-JNK-dependent anoikis upon attachment to fibronectin or integrin upregulation. The same signalling pathway is triggered by FAK inhibition or inhibiting integrin αV/β3 with Cilengitide. Thus, GT can target integrins to induce anoikis on lung epithelial cells.
UR - http://www.scopus.com/inward/record.url?scp=85052640542&partnerID=8YFLogxK
U2 - 10.1038/s41467-018-05850-w
DO - 10.1038/s41467-018-05850-w
M3 - Journal articles
AN - SCOPUS:85052640542
VL - 9
JO - Nature Communications
JF - Nature Communications
IS - 1
M1 - 3524
ER -