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Proteome profiling - Switching off IMMP2L signaling drives senescence via simultaneous metabolic alteration and blockage of cell death

ABSTRACT: quantification proteomics and neo-N-terminal peptides enrichment

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Linhui Zhai

LAB HEAD: linhui

PROVIDER: PXD006602 | Pride | 2018-06-06

REPOSITORIES: Pride

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			Action	DRS
	MaxQuant_Output.zip	Other
	SILAC_profiling_20161214_10_F1.raw	Raw
	SILAC_profiling_20161214_10_F2.raw	Raw
	SILAC_profiling_20161214_10_F3.raw	Raw
	SILAC_profiling_20161214_10_F4.raw	Raw

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Publications

Switching off IMMP2L signaling drives senescence via simultaneous metabolic alteration and blockage of cell death.

Yuan Lifeng L Zhai Linhui L Qian Lili L Huang De Ding Yi Y Xiang Handan H Liu Xiaojing X Thompson J Will JW Liu Juan J He Yong-Han YH Chen Xiao-Qiong XQ Hu Jing J Kong Qing-Peng QP Tan Minjia M Wang Xiao-Fan XF

Cell research 20180528 6

Cellular senescence is a fundamental cell fate playing a significant role throughout the natural aging process. However, the molecular determinants distinguishing senescence from other cell-cycle arrest states such as quiescence and post-mitotic state, and the specified mechanisms underlying cell-fate decisions towards senescence versus cell death in response to cellular stress stimuli remain less understood. Employing multi-omics approaches, we revealed that switching off the specific mitochond ...[more]

PMID: 29808012

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Switching off IMMP2L signaling drives senescence via simultaneous metabolic alteration and blockage of cell death.

Project description:Cellular senescence is a fundamental cell fate playing a significant role throughout the natural aging process. However, the molecular determinants distinguishing senescence from other cell-cycle arrest states such as quiescence and post-mitotic state, and the specified mechanisms underlying cell-fate decisions towards senescence versus cell death in response to cellular stress stimuli remain less understood. Employing multi-omics approaches, we revealed that switching off the specific mitochondrial processing machinery involving the peptidase IMMP2L serves as the foundation of the senescence program, which was also observed during the mammalian aging process. Mechanistically, we demonstrate that IMMP2L processes and thus activates at least two substrates, mitochondrial metabolic enzyme glycerol-3-phosphate dehydrogenase (GPD2) and cell death regulator apoptosis-inducing factor (AIF). For cells destined to senesce, concerted shutdown of the IMMP2L-GPD2 and IMMP2L-AIF signaling axes collaboratively drives the senescent process by reprogramming mitochondria-associated redox status, phospholipid metabolism and signaling network, and simultaneously blocking cell death under oxidative stress conditions.

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Transcription profiling of human HEK cells transfected with the calcium regulated gene HcARG reveals HCaRG increases renal cell migration by a TGF-alpha autocrine loop mechanism

Project description:HEK293 cells were transfected with control plasmid (pcDNA1/Neo; Invitrogen) or with the plasmid encoding HCaRG by a standard calcium phosphate co-precipitation method. The clones expressing the highest levels of HCaRG, HCaRG clone 8 and 9 were used in this experiment, while clone transfected with vector alone, Neo clone, served as controls. Stable transfectants were synchronized and grown in the presence of 10% FBS for 48 h. Total RNAs were purified with the mini RNeasy kit (Qiagen).

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Gene expression profiling of 60 pre-chemotherapy FFPE endoscopic oesophageal adenocarcinoma biopsies

Project description:Oesophageal cancer is the ninth most common cancer in the UK and accounts for 5% of all cancer deaths. The incidence of the disease in men has risen 50% in the last 25 years with the commonest pathological subtype in the West being adenocarcinoma, while in East Asia oesophageal squamous cell carcinoma predominates. Despite efforts to screen for Barrett’s oesophagus, and pre-operatively select OAC patients who are likely to benefit from potentially curative surgery, survival remains poor. The five year survival rate is less than 17% and even in early stage locoregional confined disease this figure lies between 25-35%. A significant improvement in overall survival has been demonstrated with neo-adjuvant or peri-operative chemotherapy but the optimal approach for individual patients remains unclear. A consistent finding has been that complete histopathological response to neo-adjuvant chemotherapy is a prognostic biomarker for increased survival benefit. Therefore, there is a pressing need to identify biomarkers capable of predicting response, enabling clinicians to select patients for whom neo-adjuvant therapies would be beneficial. This experiment represents gene expression profiling of 60 pre-treatment formalin-fixed paraffin embedded (FFPE) oesophageal adenocarcinoma biopsies. All patients were treated with neo-adjuvant cisplatin-based chemotherapy prior to surgical resection at the Northern Ireland Cancer Centre from 2004-2012. The aim of the experiment was to carry out functional enrichment of pathological responders and non-responders to neo-adjuvant chemotherapy in order to identify novel mechanism of drug resistance or chemo-sensitivity.

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MicroRNAs differentially expressed in MUC1 overexpressing cells

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Project description:Aberrant proteolysis by cysteine cathepsins is implicated in carcinogenesis, but knowledge of cathepsin substrates mediating tumor-promoting or suppressing effects is limited. Here we characterize tumor proteome and in vivo cathepsin substrates using cathepsin knockout mice and the RIP1-Tag2 model of pancreatic islet carcinogenesis. Applying an unbiased systems-level proteomics approach, Terminal Amine Isotopic Labeling of Substrates (TAILS), we identified cysteine cathepsin B, H, L, S, Z substrates and their cleavage sites. Among 1,935 proteins and 1,114 N-termini identified by TAILS using 8-plex iTRAQ protein labeling, 145 neo-N-termini were significantly changed in one (55%) or more knockouts suggesting a lack of direct compensation at substrate level by other cathepsins. Most affected N-termini (56-83% for different cathepsins) represented degradative cathepsin activity, whereas 17-44% of neo-N termini represented stable proteolytic products in the tumors and were enriched for extracellular proteins. We identified candidate substrates for mediating signaling roles of cysteine cathepsins in tumorigenesis.

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Hyperosmotic-induced changes in lymphoid cell gene expression

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2015-12-21 | E-GEOD-62531 | biostudies-arrayexpress

Identification of de novo LINE-1 (L1) retrotransposon integration sites in HeLa S3 cells by ATLAS-seq-neo (unselected insertions)

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