Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cisplatin-Induced Changes in Proteomic Profiles of Ovarian Cancer Cell and HaCaT Secretomes

ABSTRACT: Exogenous signals from drug-stressed cancer cells promote acquisition of a more aggressive phenotype of neighboring tumor cells. To identify extracellular signaling molecules that potentially contribute to the development of therapy resistance, we examined how cancer cell secretome changes in response to chemotherapy. We performed LC-MS/MS analysis of secretomes from several ovarian cancer cell lines representing different tumor subtypes: serous ovarian cancer cell line (OVCAR3), ovarian cystadenocarcinoma cell line (MESOV) and clear cell ovarian cancer primary culture isolated from ascites (cells 26) before and 48 hours after cisplatin treatment. In addition, we studied secretomes from keratinocyte-derived epithelial cell line HaCaT as non-cancerous “normal” cells. Functional annotation of proteins which secretion increased after cisplatin showed that these proteins were mainly associated with cluster of spliceosome.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

DISEASE(S): Malignant Neoplasm Of Ovary

SUBMITTER: Georgij Arapidi

LAB HEAD: Georgij Arapidi

PROVIDER: PXD045663 | Pride | 2024-05-29

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Sh-390-1.dat	Other
	Sh-390-1.mgf	Mgf
	Sh-390-1.mzid.gz	Mzid
	Sh-390-1.mzid_Sh-390-1.MGF	Mzid
	Sh-390-1.raw	Raw

Items per page:

1 - 5 of 98

Similar Datasets

Cisplatin-Induced Changes in Proteomic Profiles of Ovarian Cancer Cell and Fibroblast Secretomes

Project description:Exogenous signals from drug-stressed cancer cells promote acquisition of a more aggressive phenotype of neighboring tumor cells. To identify extracellular signaling molecules that potentially contribute to the development of therapy resistance, we examined how cancer cell secretome changes in response to chemotherapy. We performed LC-MS/MS analysis of conditioned media (CM) from ovarian cancer cells SKOV3 before and 48 hours after cisplatin treatment. We identified 1,820 and 784 proteins in secretomes of cancer cells treated or untreated with cisplatin, respectively. Functional annotation of proteins which secretion increased after cisplatin showed that these proteins were mainly associated with cluster of spliceosome. To investigate whether secretion of spliceosomal proteins during induction of apoptosis is a specific property of tumor cells, we compared proteomes of CM from primary culture of normal human skin fibroblasts before and 48 hours after exposure to cisplatin (IC50). A LC-MS/MS analysis revealed that most of the proteins in the CM of fibroblasts and cancer cells under normal conditions overlap, while the secretomes after therapy demonstrate much more pronounced differences. GO and KEGG enrichment analysis revealed higher abundance of cell adhesion and extracellular matrix proteins in CM of fibroblasts before chemotherapy; while lysosomal proteins and growth factors, associated with wound healing were increased after cisplatin treatment. Spliceosomal proteins were only slightly present in fibroblast CM and did not show any changes in a response to chemotherapy. We suggest that the acquisition of ovarian cancer chemoresistance might be partially mediated by extracellular spliceosomal components.

2024-05-29 | PXD019096 | Pride

SILAC Strategy for Analysis of Proteins Released To the Extracellular Medium and Penetrated

Project description:Exogenous signals from drug-stressed cancer cells accelerate the proliferation of neighboring tumor cells and promote them to acquire a more aggressive phenotype. We have recently found an exciting phenomenon: drug-stressed cancer cells secrete various spliceosomal proteins. We have observed this phenomenon both in vitro (culture media from cancer cell lines [Pavluykov M. et al.//Cancer Cell, 2018]) and in vivo (ovarian cancer ascites after chemotherapy [Shender V. et al//Mol. Сell. Proteomics, 2014]). The aim of this study was to elucidate which proteins from the extracellular vesicles can penetrate into recipient cells. SKOV3 donor cells were cultured on special medium containing isotope labeled lysine and arginine. When label inclusion was more than 98%, the cells were treated or untreated (control) with cisplatin. After 48 h, extracellular vesicles containing labeled proteins were isolated. These vesicles were added to unlabeled SKOV3 recipient cells and, after 10 or 48 h, the cells were lysed and subjected to LC-MS/MS to identify labeled proteins. We found that at least 189 heavy-labeled proteins entered recipient cells from the vesicles at 10-hour of incubation. Among them, 101 proteins were present at a higher level in cells incubated with apoptotic vesicles, and 29 proteins were present at a higher level in cells incubated with vesicles from non-apoptotic cells. Functional annotation of heavy-labeled proteins elevated in samples incubated with apoptotic vesicles revealed the highest enrichment in a cluster of spliceosome-related proteins. We suggest that the acquisition of a more aggressive phenotype of recipient cancer cells might be partially mediated by extracellular spliceosomal components.

2024-05-29 | PXD027948 | Pride

Transcription profiling by array of human A2780 ovarianc cancer cells and cisplatin resistant derivate cells treated with cisplatin or liposomal cisplatin

Project description:A2780 ovarian cancer cells and a cisplatin resistant derivate of A2780 cells, obtained from ECACC, UK, No. 93112519 [A2780] and No. 93112517 [A2780 cis] were seeded out in T-75 flasks at a density of 2x106 for A2780sens and 3x106 for A2780cis cells in 15 ml of medium and preincubated overnight. Medium was removed and 15 ml fresh medium (37M-0C) with different concentrations of cisplatin, liposomal cisplatin or empty liposomes were added and incubated for 72 h at 37M-0C in a 5% CO2 incubator. In case of A2780sens cells, 1.72 M-5M cisplatin (IC50 concentration) and in case of A2780cis cells 8.94 M-5M cisplatin (IC50 concentration) were added. Liposomal formulations contained equal cisplatin concentrations. Empty liposomes were added in the same concentration as the liposomal cisplatin, to analyze the impact of liposomal lipids (A2780sens: 0.80M-5mol lipid, A2780cis: 4.15 M-5mol lipid). After incubation, medium was removed and cells were washed thrice with 10 ml PBS. 1 ml RLT-buffer was added and cells lysates were stored at -80M-0C until RNA extraction.

2010-12-13 | E-MEXP-2840 | biostudies-arrayexpress

Effect of therapy-induced secretomes on the proteome of ovarian cancer cells

Project description:Exogenous signals from drug-stressed cancer cells promote acquisition of a more aggressive phenotype of neighboring tumor cells. Recently, we examined how cancer cell secretome changes in response to chemotherapy. Moreover, therapy-induced secretomes significantly increased resistance of cancer cells to subsequent cisplatin treatment. To elucidate how therapy-induced secretomes affect the proteomic profiles of recipient tumor cells, we incubated SKOV3 cells for 3 days with secretomes from control or dying cancer cells. Enrichment analysis of differentially abundant proteins revealed that therapy-induced secretomes provoked increase abundance of proteins involved in DNA repair and cell cycle regulation. These findings demonstrate that under stress condition cancer cells can secrete signaling molecules into the extracellular space and contribute to the emergence of tumor chemoresistance during short time period.

2024-05-29 | PXD027794 | Pride

Analysis of gene expression changes in response to hypoxia and/or cisplatin in A2780 and A2780cis cells

Project description:The aim of this experiment was to evaluate the changes in gene expression in response to hypoxia and/or cisplatin in an ovarian cancer cell line model. A2780 (cisplatin-sensitive) and A2780cis (cisplatin-resistant) cell lines were treated with cisplatin in normoxia or hypoxia (0.5% O2) for 72 hours. RNA was extracted from three independent biological replicates for each condition: A2780 (normoxia, untreated); A2780 (hypoxia, untreated); A2780 (normoxia, cisplatin); A2780cis (hypoxia, cisplatin), A2780cis (normoxia, untreated); A2780cis (hypoxia, untreated); A2780cis (normoxia, cisplatin); A2780cis (hypoxia, cisplatin) and interrogated on Affymetrix Human Gene ST 1.0 arrays.

2016-01-15 | E-MTAB-3645 | biostudies-arrayexpress

Effect of malignant ascites before and after therapy on the proteome of ovarian cancer cells

Project description:Ovarian cancer is characterized by transcoelomic metastasis into the peritoneal cavity. The peritoneal malignant ascites is enriched with ovarian cancer cells and a small amount of tumor-associated immune cells which create a unique microenvironment actively contributing to progression of the disease. However, it remains unclear how cancer cells communicate to its local environment under the influence of chemotherapy. To address this issue, we performed LC-MS/MS analyses of several primary cultures of ovarian cancer cells from chemonaive malignant ascites incubated for 3 days with autologous pre- or post-chemotherapy ascitic fluids. Enrichment analysis identified prominent upregulation of proteins associated with pathways of DNA repair and cell cycle regulation in tumor cells incubated with ascitic fluids after chemotherapy. Consistently with these data, ascites after therapy increased the resistance of ovarian cancer cells to cisplatin. These findings demonstrate that under stress condition cancer cells can secrete signaling molecules into the extracellular space and contribute to the emergence of tumor chemoresistance during short time period.

2024-05-29 | PXD045647 | Pride

Innate immune agonist, dsRNA, induces apoptosis in ovarian cancer cells and enhances the potency of cytotoxic chemotherapeutics

Project description:This study aimed at characterizing the effect of the innate immune agonist, dsRNA, on ovarian cancer cell lines and ascites-derived ovarian cancer cells. DsRNA stimulation revealed two sub-populations of ovarian cancer cells, dsRNA sensitive and dsRNA resistant, that could be categorized based upon dsRNA-induced dsRNA receptor expression. Human ovarian cancer cell lines were treated with pI:pC and compared against untreated cells.

2012-04-28 | E-GEOD-33342 | biostudies-arrayexpress

Gene Expression Profile of Cisplatin Resistance in Ovarian Cancer Cell Lines

Project description:To determine the signaling networks that are dysregulated in platinum-resistant ovarian cancer, gene expression data were obtained from, and compared between, the ovarian cancer cell line, A2780, and its cisplatin-resistant derivative, A2780cis. Gene expression data from a cisplatin-sensitive ovarian cancer cell line (A2780) were collected and compared to gene expression data from a cisplatin-resistant cell line (A2780cis). 6 independent experiments were completed for both the sensitive and resistant cell lines.

2011-11-05 | E-GEOD-33482 | biostudies-arrayexpress

Genomic profiling of EOC organoids: low-coverage whole-genome sequencing

Project description:Organoids were established from patients with ovarian cancer. DNA was extracted from organoids and primary tissue to investigate whether organoids retain the same genomic abnormalities and disease-associated features.

2020-12-01 | E-MTAB-8636 | biostudies-arrayexpress

Resistance of primary ovarian cancer cells to oncolytic adenoviruses

Project description:This SuperSeries is composed of the following subset Series: GSE15350: Resistance of primary ovarian cancer cells to oncolytic adenoviruses part1 of 2 GSE15351: Resistance of primary ovarian cancer cells to oncolytic adenoviruses part2 of 2 Refer to individual Series

2009-04-01 | E-GEOD-15473 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data