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Interaction of Discoidin Domain Receptor 1 with a 14-3-3-Beclin-1-Akt1 Complex Modulates Glioblastoma Therapy Sensitivity.

Abstract：

:Glioblastoma (GBM) is highly refractory to therapy and associated with poor clinical outcome. Here, we reveal a critical function of the promitotic and adhesion-mediating discoidin domain receptor 1 (DDR1) in modulating GBM therapy resistance. In GBM cultures and clinical samples, we show a DDR1 and GBM stem cell marker co-expression that correlates with patient outcome. We demonstrate that inhibition of DDR1 in combination with radiochemotherapy with temozolomide in GBM models enhances sensitivity and prolongs survival superior to conventional therapy. We identify a 14-3-3-Beclin-1-Akt1 protein complex assembling with DDR1 to be required for prosurvival Akt and mTOR signaling and regulation of autophagy-associated therapy sensitivity. Our results uncover a mechanism driven by DDR1 that controls GBM therapy resistance and provide a rationale target for the development of therapy-sensitizing agents.

journal_name

Cell Rep

journal_title

Cell reports

authors

Vehlow A,Klapproth E,Jin S,Hannen R,Hauswald M,Bartsch JW,Nimsky C,Temme A,Leitinger B,Cordes N

doi

10.1016/j.celrep.2019.02.096

subject

Has Abstract

pub_date

2019-03-26 00:00:00

pages

3672-3683.e7

issue

13

issn

2211-1247

pii

S2211-1247(19)30282-7

journal_volume

26

pub_type

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