Role of PAEP/glycodelin in NSCLC
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA475100 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression profiling of NSCLC tumors with distinct PAEP expression suggested several pathways, which might be involved in the regulation of PAEP/glycodelin expression.
2018-11-12 | GSE115457 | GEO
Project description:The function of glycodelin A in the endometrium, during the menstrual cycle, and before or during pregnancy is well characterized. Numerous studies have investigated the highly pleiotropic effects and the modulation of different leukocytes upon glycodelin interaction. In NSCLC, the function of glycodelin is not known, yet. While it was shown to be highly expressed in lung tumor tissue compared to normal lung, the functionality and possible immunomodulating characteristics remain to be described.
2023-01-09 | GSE222124 | GEO
Project description:We compared H1975 and 2106T cells treated with PAEP/glycodelin expression inducing substances and the corresponding contol treated cells. Gene expression profiling of H1975 and 2106T cells with induced PAEP/glycodelin expression might give hints on several pathways regulating this activated expression.
2018-11-12 | GSE115456 | GEO
Project description:Gene expression profiling of two NSCLC cell lines treated with PAEP/glycodelin expression stimulating substances
| PRJNA475103 | ENA
Project description:In cancer, proto-oncogenes are often altered by genomic amplification. Recent studies have highlighted a role for PDGFRA as an oncogene in non-small cell lung cancer. To characterize 4q12 copy number status in NSCLC, both previously published (Weir et al. PMID 17982442) and unpublished Affymetrix 250K SNP array data for 733 NSCLC samples (628 primary samples, 105 cell lines) were evaluated for copy number aberrations. 4q12 amplifications overlapping the PDGFRA/KIT locus were observed in 31 (4.2%) NSCLC samples. SNP array and FISH analysis indicate that 4q12 is amplified in 3-7% of lung adenocarcinomas and 8-10% of lung squamous cell carcinomas. In addition, the NSCLC cell line NCI-H1703 exhibits focal amplification of PDGFRA and is dependent on PDGFRα activity for cell growth. Treatment of NCI-H1703 cells with PDGFRA-specific shRNAs or with the PDGFRα/KIT small molecule inhibitors imatinib or sunitinib leads to cell growth inhibition. However, these observations do not extend to NSCLC cell lines with lower-amplitude and broader gains of chromosome 4q. Together these observations implicate PDGFRA and KIT as potential oncogenes in NSCLC, but further study is needed to define the specific characteristics of those tumors that could respond to PDGFRα/KIT inhibitors.
2009-09-15 | GSE17429 | GEO
Project description:Non-coding RNAs are critical players in non-small cell lung cancer (NSCLC). In the present study, we investigate the role of H/ACA box snoRNA and snoRNA-bound ribonucleoproteins (RNP) in the tumorigenesis of NSCLC.
2020-11-17 | GSE160928 | GEO
Project description:Protein glycosylation plays a fundamental role in a multitude of biological processes, and the associated aberrant expression of glycoproteins in cancer has made them attractive targets as biomarkers and therapeutic targets. In this study, we examined differentially expressed glycoproteins in cell lines derived from three different states of lung tumorigenesis: an immortalized bronchial epithelial cell (HBE) line, a non-small cell lung cancer (NSCLC) cell line harboring an activation KRAS mutation and a NSCLC cell line harboring an EGFR activation deletion. Mutations in KRAS and EGFR are two common, distinct, non-overlapping genomic alterations in NSCLC. Using a Triple SILAC proteomic quantification strategy paired with hydrazide chemistry N-linked glycopeptide enrichment, we identified 118 quantifiable glycopeptides in the 3 cell lines derived from 82 glycoproteins. Proteomic profiling revealed that 27 (24%) of the glycopeptides overexpressed in both of the NSCLC cell lines with 6 of the glycopeptides overexpressed only in the EGFR mutant cells and 19 of the glycopeptides overexpressed only in the KRAS mutant cells.
2015-12-10 | PXD001999 | Pride
Project description:Protein glycosylation plays a fundamental role in a multitude of biological processes, and the associated aberrant expression of glycoproteins in cancer has made them attractive targets as biomarkers and therapeutic targets. In this study, we examined differentially expressed glycoproteins in cell lines derived from three different states of lung tumorigenesis: an immortalized bronchial epithelial cell (HBE) line, a non-small cell lung cancer (NSCLC) cell line harboring an activation KRAS mutation and a NSCLC cell line harboring an EGFR activation deletion. Mutations in KRAS and EGFR are two common, distinct, non-overlapping genomic alterations in NSCLC. Using a Triple SILAC proteomic quantification strategy paired with hydrazide chemistry N-linked glycopeptide enrichment, we identified 118 quantifiable glycopeptides in the 3 cell lines derived from 82 glycoproteins. Proteomic profiling revealed that 27 (24%) of the glycopeptides overexpressed in both of the NSCLC cell lines with 6 of the glycopeptides overexpressed only in the EGFR mutant cells and 19 of the glycopeptides overexpressed only in the KRAS mutant cells.
2016-03-10 | MSV000079569 | MassIVE
Project description:34 NSCLC cell lines were transcriptionally profiled against a reference mix of 45 NSCLC cell lines to look subtype specific differential gene expression 34 individual cell lines were compared to a reference mix consiting of 45 NSCLC cell lines
2013-01-18 | E-GEOD-43567 | biostudies-arrayexpress
Project description:Bidkhori2012 - EGFR signalling in NSCLC
The paper describes and compares two models on EGFR signalling between normal and NSCLC cells. Moreover, it is shown that ERK (MAPK), STAT and Akt factor's activation pattern are different between normal and NSCLA models. This model corresponds to EGFR signalling in NSCLA cells.
Created by The MathWorks, Inc. SimBiology tool, Version 3.3
This model is described in the article:
Modeling of tumor progression in NSCLC and intrinsic resistance to TKI in loss of PTEN expression.
Bidkhori G, Moeini A, Masoudi-Nejad A
PloS one [2012, 7(10):e48004]
Abstract:
EGFR signaling plays a very important role in NSCLC. It activates Ras/ERK, PI3K/Akt and STAT activation pathways. These are the main pathways for cell proliferation and survival. We have developed two mathematical models to relate to the different EGFR signaling in NSCLC and normal cells in the presence or absence of EGFR and PTEN mutations. The dynamics of downstream signaling pathways vary in the disease state and activation of some factors can be indicative of drug resistance. Our simulation denotes the effect of EGFR mutations and increased expression of certain factors in NSCLC EGFR signaling on each of the three pathways where levels of pERK, pSTAT and pAkt are increased. Over activation of ERK, Akt and STAT3 which are the main cell proliferation and survival factors act as promoting factors for tumor progression in NSCLC. In case of loss of PTEN, Akt activity level is considerably increased. Our simulation results show that in the presence of erlotinib, downstream factors i.e. pAkt, pSTAT3 and pERK are inhibited. However, in case of loss of PTEN expression in the presence of erlotinib, pAkt level would not decrease which demonstrates that these cells are resistant to erlotinib.
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2024-09-02 | BIOMD0000000453 | BioModels