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00085472can133430-sup-fig_2.pdf (327.49 kB)

Supplementary Figure 2 from hMOB3 Modulates MST1 Apoptotic Signaling and Supports Tumor Growth in Glioblastoma Multiforme

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posted on 2023-03-30, 22:51 authored by Fengyuan Tang, Lei Zhang, Gongda Xue, Debby Hynx, Yuhua Wang, Peter D. Cron, Christian Hundsrucker, Alexander Hergovich, Stephan Frank, Brian A. Hemmings, Debora Schmitz-Rohmer

PDF file - 323KB, Supplemental Figure 2. hMOB3 specifically interacts with MST1.

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ARTICLE ABSTRACT

New therapeutic targets are needed that circumvent inherent therapeutic resistance of glioblastoma multiforme (GBM). Here, we report such a candidate target in the uncharacterized adaptor protein hMOB3, which we show is upregulated in GBM. In a search for its biochemical function, we found that hMOB3 specifically interacts with MST1 kinase in response to apoptotic stimuli and cell–cell contact. Moreover, hMOB3 negatively regulated apoptotic signaling by MST1 in GBM cells by inhibiting the MST1 cleavage-based activation process. Physical interaction between hMOB3 and MST1 was essential for this process. In vivo investigations established that hMOB3 sustains GBM cell growth at high cell density and promotes tumorigenesis. Our results suggest hMOB3 as a candidate therapeutic target for the treatment of malignant gliomas. Cancer Res; 74(14); 3779–89. ©2014 AACR.

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    Cancer Research

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    BiochemistryProtein/protein interactionsBiomarkersCell Death And SenescenceCaspasesCell SignalingCns CancersDrug MechanismsCellular responses to anticancer drugsDrug-mediated stimulation of cell death pathwaysOncogenes & Tumor Suppressors

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