Proteomics

Dataset Information

0

Modulation of glioma cell proteome by Delta-24-RGD adenovirus (48hpi)

ABSTRACT: Glioblastoma multiforme (GBM) is the most common and aggressive type of malignant glioma. Oncolytic adenoviruses are being modified to exploit the aberrant expression of proteins in tumor cells to enhance tumor tropism and glioma-selective replication. E1A mutant adenovirus Delta-24-RGD has shown favorable toxicity profile and remarkable efficacy in a first-in-human phase I clinical trial. However, the comprehensive modulation of glioma metabolism in response to Delta-24-RGD infection is poorly understood. Integrating mass spectrometry based-quantitative proteomics, physical and functional interaction data, and biochemical approaches, we conducted a cell-wide study of intracellular and secreted glioma proteomes at late stage of Delta-24-RGD infection, when prominent autophagy has been described.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Astrocyte

DISEASE(S): Glioblastoma

SUBMITTER: Enrique Santamaría  

LAB HEAD: Enrique Santamaria

PROVIDER: PXD010256 | Pride | 2018-12-11

REPOSITORIES: Pride

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0h_1092_24y48hpi04.05.181.group Other
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0h_1092_24y48hpi04.05.181.wiff.scan Wiff
0h_1092_24y48hpi04.05.181__FDR.xlsx Xlsx
0h_2092_24y48hpi04.05.182.group Other
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Publications

Oncolytic adenovirus Delta-24-RGD induces a widespread glioma proteotype remodeling during autophagy.

González-Morales Andrea A   Zabaleta Aintzane A   García-Moure Marc M   Alonso Marta M MM   Fernández-Irigoyen Joaquín J   Santamaría Enrique E  

Journal of proteomics 20181129

Adenovirus Delta-24-RGD has shown a remarkable efficacy in a phase I clinical trial for glioblastoma. Delta-24-RGD induces autophagy in glioma cells, however, the molecular derangements associated with Delta-24-RGD infection remains poorly understood. Here, proteomics was applied to characterize the glioma metabolic disturbances soon after Delta-24-RGD internalization and late in infection. Minutes post-infection, a rapid survival reprogramming of glioma cells was evidenced by an early c-Jun act  ...[more]

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