Proteomics

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MET-dependent modulation of cellular responses to ionizing radiation by quantitative phosphoproteomics

ABSTRACT: Increasing evidence suggests that inhibiting growth factor receptor tyrosine kinases (RTKs) signaling may modulate cellular responses to DNA-damaging agents widely used in cancer treatment. In that respect, the MET RTK is deregulated in abundance and/or activity in a variety of human tumors. Using two proteomic techniques, we explored how the MET inhibitor tepotinib modulates global cellular phosphorylation response to ionizing radiation (IR). Following an immunoaffinity-based phosphoproteomic discovery survey we selected candidate phosphorylation sites for extensive characterization by targeted proteomics focusing on phosphosites that consist of the SQ motif recognized by the PIKK-related kinases ATM, ATR and PRKDC. Several substrates of the DNA damage response (DDR) were confirmed to be modulated by sequential MET inhibition and IR, or MET inhibition alone.

INSTRUMENT(S): LTQ Orbitrap Velos, Q TRAP

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Ariel Bensimon  

LAB HEAD: Ruedi Aebersold

PROVIDER: PXD009433 | Pride | 2020-05-15

REPOSITORIES: Pride

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Publications

Deciphering MET-dependent modulation of global cellular responses to DNA damage by quantitative phosphoproteomics.

Bensimon Ariel A   Koch Jonas P JP   Francica Paola P   Roth Selina M SM   Riedo Rahel R   Glück Astrid A AA   Orlando Eleonora E   Blaukat Andree A   Aebersold Daniel M DM   Zimmer Yitzhak Y   Aebersold Ruedi R   Medová Michaela M  

Molecular oncology 20200513 6

Increasing evidence suggests that interference with growth factor receptor tyrosine kinase (RTK) signaling can affect DNA damage response (DDR) networks, with a consequent impact on cellular responses to DNA-damaging agents widely used in cancer treatment. In that respect, the MET RTK is deregulated in abundance and/or activity in a variety of human tumors. Using two proteomic techniques, we explored how disrupting MET signaling modulates global cellular phosphorylation response to ionizing radi  ...[more]

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