Dataset Information

Germ-free mouse ileum iTRAQ shotgun LC-MSMS

ABSTRACT: Shotgun proteomics of normal versus germ-free mouse terminal ileum. 39 mice. Male and female. BALBc and C57BL10. The samples were labeled using iTRAQ 8plex and analyzed using a nano-LC-LTQ-Orbitrap-Velos-MSMS. This is the proteomics data from an n-omics project.

OTHER RELATED OMICS DATASETS IN: PRJNA377762

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Ileum

SUBMITTER: Aleksandra Nita-Lazar

LAB HEAD: Aleksandra Nita-Lazar

PROVIDER: PXD003177 | Pride | 2017-10-04

REPOSITORIES: Pride

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Publications

Multi-omics Comparative Analysis Reveals Multiple Layers of Host Signaling Pathway Regulation by the Gut Microbiota.

Manes Nathan P NP Shulzhenko Natalia N Nuccio Arthur G AG Azeem Sara S Morgun Andrey A Nita-Lazar Aleksandra A

mSystems 20170901 5

The bodies of mammals are hosts to vast microbial communities composed of trillions of bacteria from thousands of species, whose effects on health and development have begun to be appreciated only recently. In this investigation, an integrated analysis combining proteomics and transcriptomics was used to quantitatively compare the terminal ilia from conventional and germfree mice. Female and male mice responded similarly to the microbiota, but C57BL/10A mice responded more strongly than BALB/c m ...[more]

PMID: 29085914

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Project description:Although malignant gliomas frequently show aberrant activation of the mammalian target of rapamycin (mTOR), mTOR inhibitors have performed poorly in clinical trials. Besides regulating cell growth and translation, mTOR controls the initiation of autophagy. By recycling cellular components, autophagy can mobilize energy resources, and has thus been attributed cancer-promoting effects. Here, we asked whether the activation of autophagy represents an escape mechanism to pharmacological mTOR inhibition, and explored co-treatment with mTOR and autophagy inhibitors as a therapeutic strategy. Mimicking conditions of the glioma microenvironment, glioma cells were exposed to nutrient starvation and hypoxia. Following treatment with mTOR inhibitor torin2 or rapamycin, and autophagy inhibitors bafilomycin A1 or MRT68921, we analyzed autophagic activity, cell growth, viability and oxygen consumption. Changes in global proteome were quantified by mass spectrometry. In the context of hypoxia and starvation, autophagy was strongly induced in glioma cells, and further increased by mTOR inhibition. While torin2 enhanced glioma cell survival, co-treatment with torin2 and bafilomycin A1 failed to promote cell death. Importantly, treatment with bafilomycin A1 alone also protected glioma cells from cell death. Mechanistically, both compounds significantly reduced glioma growth and oxygen consumption. Mass spectrometry analysis showed that bafilomycin A1 induced broad changes in the cellular proteome. More specifically, proteins downregulated by bafilomycin A1 were associated with the mitochondrial respiratory chain and ATP synthesis. Taken together, our results show that activation of autophagy does not account for the cytoprotective effects of mTOR inhibition in our in vitro model of the glioma microenvironment. Our proteomic findings suggest that the pharmacological inhibition of autophagy induces extensive changes in the cellular proteome that can support glioma cell survival under nutrient-deplete and hypoxic conditions. These findings provide a novel perspective on the complex role of autophagy in gliomas and may have implications for the design of future trials.

Dataset Information

Germ-free mouse ileum iTRAQ shotgun LC-MSMS

Publications

Multi-omics Comparative Analysis Reveals Multiple Layers of Host Signaling Pathway Regulation by the Gut Microbiota.

Similar Datasets

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