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LC-MS/MS of Rab21 pull-down or control sample

ABSTRACT: LC-MS/MS of Rab21 pull-down or control sample from 786-O cells

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Kidney Cell

DISEASE(S): Kidney Cancer

SUBMITTER: Gao Song

LAB HEAD: Gao Song

PROVIDER: PXD033104 | Pride | 2023-10-24

REPOSITORIES: Pride

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Publications

MFN2 suppresses clear cell renal cell carcinoma progression by modulating mitochondria-dependent dephosphorylation of EGFR.

Luo Li L Wei Denghui D Pan Yihui Y Wang Qiu-Xia QX Feng Jian-Xiong JX Yu Bing B Kang Tiebang T Luo Junhang J Yang Jiefeng J Gao Song S

Cancer communications (London, England) 20230628 7

<h4>Background</h4>Clear cell renal cell carcinoma (ccRCC) is the most lethal renal cancer. An overwhelming increase of patients experience tumor progression and unfavorable prognosis. However, the molecular events underlying ccRCC tumorigenesis and metastasis remain unclear. Therefore, uncovering the underlying mechanisms will pave the way for developing novel therapeutic targets for ccRCC. In this study, we sought to investigate the role of mitofusin-2 (MFN2) in supressing ccRCC tumorigenesis ...[more]

PMID: 37378422

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Potential proteins interacted with S100A11

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EP300 promotes ferroptosis via HSPA5 acetylation in pancreatic cancer

Project description:Ferroptosis is a form of regulated cell death characterized by oxidative injury-induced lipid peroxidation. However, the detailed protein post-translational modification regulatory mechanism of ferroptosis remains largely unknown. Here, we report that E1A binding protein P300 (EP300) acetyltransferase promotes ferroptosis in human pancreatic ductal adenocarcinoma (PDAC) cells via the acetylation of heat shock protein family A (Hsp70) member 5 (HSPA5, also known as GRP78 or BIP) on the site of K353. Acetylated HSPA5 loses its ability to inhibit lipid peroxidation and subsequent ferroptotic cell death. Genetic or pharmacological inhibition of EP300-mediated HSPA5 acetylation on K353 increases PDAC cell resistance to ferroptosis. Moreover, histone deacetylase 6 (HDAC6) limits HSPA5 acetylation and subsequent ferroptosis.

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LC-MS/MS of extracellular vesicles from murine osteosarcoma cell line K7 and K7M2

Project description:Extracellular vesicles have been shown to be highly enriched in proteins with various functions, including organotropic metastasis. To identify possible protein cargos involved in regulating mestastatic potential of osteosarcoma cell line, we performed quantitative mass spectrometry analysis of EVs from highly metastatic K7M2 cells and poorly metastatic parental K7 cells.

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BRBseq performed on 786-O cells treated with 2 inhibitors of protein kinase CK2, CX4945 and AB668

Project description:786-O cells (150, 000) were treated for 24h with DMSO, 5 µM of CX4945 or AB668. Total RNA was extracted from treated cells using the MirVana PARIS kit (Thermofisher). The 3′ Bulk RNA Barcoding and sequencing (BRB-seq) experiments were performed at the Research Institute for Environmental and Occupational Health (Irset, Rennes, France) according to the published protocol (Alpern et al., 2019). Sequencing was perfomred by SiLicium.

2023-05-27 | E-MTAB-12776 | biostudies-arrayexpress

Expression data from 786-O renal cell cancer cells treated with pentamidine

Project description:While early stages of clear cell renal cell carcinoma (ccRCC) are curable, survival outcome for metastatic ccRCC remains poor. The purpose of the current study was to apply a new individualized bioinformatics analysis (IBA) strategy to these transcriptome data in conjunction with Gene Set Enrichment Analysis of the Connectivity Map (C-MAP) database to identify and reposition FDA-approved drugs for anti-cancer therapy. We demonstrated that one of the drugs predicted to revert the RCC gene signature towards normal kidney, pentamidine, is effective against RCC cells in culture and in a RCC xenograft model. Most importantly, pentamidine slows tumor growth in the 786-O human ccRCC xenograft mouse model. To determine which genes are regulated by pentamidine in a human RCC cell line, 786-O, we treated these cells with pentamidine and performed transcriptional profiling analysis. We used microarrays to determine the set of genes regulated by pentamidine in 786-O renal cell cancer cells. Total RNA was isolated from 786-O cells treated with 25 Î¼M pentamidine or vehicle control (DMSO) for 6 hours and hybridized to Affymetrix microarrays.

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BRBseq performed on tumoroids and corresponding renal tumor tissues

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Cellular and molecular characterization of the altered metabolism in RCC

Project description:RCC cells (786-O) were transfected with VHL. The parental cell line should be compared to the transfectant (+ VHL) under nomoxia as well as under hypoxia conditions. We want to distinct the VHL-mediated gene expression from the hypoxia-mediated and study the influence of both on the cellular metabolism. RNA of VHL-negative 786-O RCC cell line and VHL-transfectants incubated during normoxia and hypoxia conditions were analysed by cDNA microarray.

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IGR_MESSAI_CCRCC_HIF2

Project description:The aim of the present study was to investigate the potential role of HIF-2a in regulating RCC susceptibility to natural killer (NK) cell-mediated killing. We demonstrated that the RCC cell line 786-O with mutated VHL was resistant to NK-mediated lysis as compared to the VHL corrected cell line (WT7). This resistance was independent of immunological synapse formation and NK ligand expression but was found to be reliant on HIF-2a stabilization in 786-0 cells. In order to elucidate the molecular basis of HIF-2a-induced impairment of NK-mediated killing, we performed global gene analysis using DNA microarray. Three candidate genes (ANGPTL4, ADM and ITPR1) were selected on the basis of their fold change and their involvement in cell death and survival. SiRNA targeting of these genes revealed that only ITPR1 silencing resulted in a significant increase of 786-O susceptibility to NK-mediated lysis. Using gene silencing of HIF2-a and chromatin immunoprecipitation assay, we showed for the first time that ITPR1 was a direct novel target of HIF2-a. Notably, a strong and significant correlation was found between ITPR1and HIF2-a staining in RCC patients. Transcriptional profiling of ITPR1silenced RCC cells indicated that several important genes involved in cell survival and apoptosis were differentially regulated. Using ITPR1 silenced Renca cells, we further found that ITPR1 was involved in the control of tumor progression. Moreover ITPR1 targeting combined with NK depletion significantly enhanced tumor growth as compared to ITPR1 knocked down Renca xenografts. Our data provide insights into the link between HIF-2a, ITPR1-related pathway and natural immunity and suggest a role of the HIF2/ITPR1 axis in regulating RCC cell survival.

2014-01-11 | E-MTAB-1802 | biostudies-arrayexpress

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