Dataset Information

Proteome and Translatome of SARS-CoV-2 infected cells

ABSTRACT: Cells were infected with SARS-CoV-2 and profiled for translatome and proteome after 2,6,10 and 24 hours

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Colon

DISEASE(S): Colon Cancer

SUBMITTER: Kevin Klann

LAB HEAD: Christian Münch

PROVIDER: PXD017710 | Pride | 2020-07-20

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	20200219_KKL_SARS_CoV2_pool1_F.msf	Msf
	20200219_KKL_SARS_CoV2_pool1_F1.raw	Raw
	20200219_KKL_SARS_CoV2_pool1_F2.raw	Raw
	20200219_KKL_SARS_CoV2_pool1_F3.raw	Raw
	20200219_KKL_SARS_CoV2_pool1_F4.raw	Raw

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Publications

Proteomics of SARS-CoV-2-infected host cells reveals therapy targets.

Bojkova Denisa D Klann Kevin K Koch Benjamin B Widera Marek M Krause David D Ciesek Sandra S Cinatl Jindrich J Münch Christian C

Nature 20200514 7816

A new coronavirus was recently discovered and named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Infection with SARS-CoV-2 in humans causes coronavirus disease 2019 (COVID-19) and has been rapidly spreading around the globe<sup>1,2</sup>. SARS-CoV-2 shows some similarities to other coronaviruses; however, treatment options and an understanding of how SARS-CoV-2 infects cells are lacking. Here we identify the host cell pathways that are modulated by SARS-CoV-2 and show that inhib ...[more]

PMID: 32408336

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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.