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Surface proteome profiling of p53-restorable murine liver cancer cells

ABSTRACT: Characterization of the surface proteome changes between proliferating and senescent liver cancer cells induced by p53 restoration.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

SUBMITTER: Yu-Jui Ho

LAB HEAD: Scott Lowe

PROVIDER: PXD034465 | Pride | 2023-03-11

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	1398DC_S1_Uniprot_Mouse_updated_FINAL.sf3	Other
	1486HC_S1_Mouse_Uniprot_20220602_Final.sf3	Other
	PRO_1.raw	Raw
	PRO_2.raw	Raw
	PRO_4.raw	Raw

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1 - 5 of 21

Publications

Senescence Rewires Microenvironment Sensing to Facilitate Antitumor Immunity.

Chen Hsuan-An HA Ho Yu-Jui YJ Mezzadra Riccardo R Adrover Jose M JM Smolkin Ryan R Zhu Changyu C Woess Katharina K Bernstein Nicholas N Schmitt Georgia G Fong Linda L Luan Wei W Wuest Alexandra A Tian Sha S Li Xiang X Broderick Caroline C Hendrickson Ronald C RC Egeblad Mikala M Chen Zhenghao Z Alonso-Curbelo Direna D Lowe Scott W SW

Cancer discovery 20230201 2

Cellular senescence involves a stable cell-cycle arrest coupled to a secretory program that, in some instances, stimulates the immune clearance of senescent cells. Using an immune-competent liver cancer model in which senescence triggers CD8 T cell-mediated tumor rejection, we show that senescence also remodels the cell-surface proteome to alter how tumor cells sense environmental factors, as exemplified by type II interferon (IFNγ). Compared with proliferating cells, senescent cells upregulate ...[more]

PMID: 36302222

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Integrative membrane proteome analysis of High and Low-metastatic Lung Cancers

Project description:Membrane proteins play critical roles between the tumor cells and the extra-cellular matrix (ECM) during metastasis. In this study, we performed quantitative proteomic analysis of membrane proteins from two human giant-cell lung carcinoma cell strains, low- (95C) and high-(95D) metastatistic cell lines, and combining with microRNA analysis, we identified a multi-omics regulation module.

2020-08-18 | PXD016912 | Pride

An Informatic Approach to Chimeric Antigen Receptor Discovery Integrates Proteomics and Transcriptomics to Identify Novel Combinatorial Pairs

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2017-10-24 | PXD007552 | Pride

Legionella pneumophila proteome

Project description:Legionella pneumophila cells were harvested during exponential growth (RP) and stationary growth (TP). VBNC cells were also anylzed. Protein subfractions were studied.

2015-11-13 | PXD001926 | Pride

Nuclear-capture of endosomes drives depletion of nuclear G-actin to promote SRF/MRTF gene expression and cancer cell invasiveness (part 2: Surface and Nuclear Proteomes)

Project description:Signals are relayed from receptor tyrosine kinases (RTKs) at the cell surface to effector systems in the cytoplasm and nucleus, and coordination of this process is important for the execution of migratory phenotypes, such as cell scattering and invasion. The endosomal system influences how RTK signalling is coded, but the ways in which it transmits these signals to the nucleus to influence gene expression are not yet clear. Here we show that an RTK, MET promotes Rab17- and clathrin-dependent endocytosis of EphA2, another RTK, followed by centripetal transport of EphA2-positive endosomes. EphA2 then mediates physical capture of endosomes on the outer surface of the nucleus; a process involving interaction between the nuclear import machinery and a nuclear localisation sequence in EphA2’s cytodomain. Nuclear capture of EphA2 promotes RhoG-dependent phosphorylation of the actin-binding protein, cofilin to oppose nuclear import of G-actin. The resulting depletion of nuclear G-actin drives transcription of Myocardin-related transcription factor (MRTF)/serum-response factor (SRF)-target genes to implement cell scattering and the invasive behaviour of cancer cells.

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NOTCH1 mediates a reciprocal switch between two distinct secretomes during senescence

Project description:Senescence, a persistent form of cell cycle arrest, is often associated with a diverse secretome, which provides complex downstream functionality for senescent cells within the tissue microenvironment. We show that oncogene-induced senescence (OIS) is accompanied by a dynamic fluctuation of NOTCH1 activity, which drives a TGF-β-rich secretome, whilst suppressing the senescence-associated pro-inflammatory secretome through inhibition of C/EBPβ. NOTCH1 and NOTCH1-driven TGF-β contribute to ‘lateral induction of senescence’ through a juxtacrine NOTCH-JAG1 pathway. In addition, NOTCH1 inhibition during senescence facilitates upregulation of pro-inflammatory cytokines, promoting lymphocyte recruitment and senescence surveillance in vivo. Because enforced activation of NOTCH1 signalling confers a near mutually exclusive secretory profile compared to typical senescence, our data collectively indicate that the dynamic alteration of NOTCH1 activity during senescence dictates a functional balance between these two distinct secretomes: one representing TGF-β and the other pro-inflammatory cytokines, highlighting that NOTCH1 is a temporospatial controller of secretome composition.

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Comparing the plasma membrane proteins of Nek1+/+ and Nek1Kat2J/Kat2J MEFs

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2021-08-06 | PXD027493 | Pride

Structural surfaceomics of Nomo-1 using PhoX cross-linker with timsTOF

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2023-10-04 | PXD035591 | Pride

VEGFR N-glycosylation

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