Gene expression profile in Non-Small Cell Lung Cancer
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Viglietto Giuseppe
PROVIDER: S-ECPF-TABM-1192 | biostudies-other |
REPOSITORIES: biostudies-other
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Project description:Integrins are involved in extracellular and intracellular signaling and are often aberrantly expressed in tumors. Integrin beta 2 (ITGB2) has previously been demonstrated to be correlated with the host defense. However, the expression profile and role of ITGB2 in non-small-cell lung cancer (NSCLC) remain unclear. Here, we found that the genetic alterations in ITGB2 was predominated by gene mutation and copy number deletion using cBioPortal analysis, and its expression was downregulated in the NSCLC tissues, as validated by the UALCAN, TCGA, and GEO databases and our tissue samples. Kaplan-Meier (KM) plotter analysis revealed that patients with a lower ITGB2 expression had a shorter overall survival (OS) time (p = 0.01). Moreover, 1089 differentially expressed genes (DEGs) in the NSCLC tissues were screened using the TCGA database. The GO and KEGG enrichment analysis showed that the DEGs were closely associated with immune processes and cell adhesion. The protein-protein interaction (PPI) network revealed that 10 of 15 EMT-related genes among the DEGs might lead to the metastasis of NSCLC. Concomitantly, the expression of ITGB2 was positively correlated with the infiltration of Treg cells and Myeloid-derived suppressor cells (MDSC). Biologically, the ectopic expression of ITGB2 significantly inhibited the proliferation and metastasis of NSCLC cells. Mechanistically, we demonstrated that ITGB2 suppressed the expression of N-cadherin, Vimentin, Slug, Snail, and Twist, while it promoted E-cadherin expression, according to gain-of-function studies. In conclusion, ITGB2 can inhibit the proliferation and migration of NSCLC cells, leading to a poor prognosis, via epithelial-mesenchymal transition (EMT) signaling.
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Project description:Lung cancer is the leading cause of cancer-related deaths worldwide. Although several therapeutic strategies have been employed to curb lung cancer, the survival rate is still poor owing to the development of drug resistance. The mechanisms underlying drug resistance development are incompletely understood. Here, we aimed to identify the common signaling pathways involved in drug resistance in non-small cell lung cancer (NSCLC). Three published transcriptome microarray data were downloaded from the Gene Expression Omnibus (GEO) database comprising different drug-resistant cell lines and their parental cell lines. Differentially expressed genes (DEGs) were identified and used to perform Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. An overlapping analysis was performed for KEGG pathways enriched from all the three datasets to identify the common signaling pathways. As a result, we found that metabolic pathways, ubiquitin-mediated proteolysis, and mitogen-activated protein kinase (MAPK) signaling were the most aberrantly expressed signaling pathways. The knockdown of nicotinamide phosphoribosyltransferase (NAMPT), the gene involved in metabolic pathways and known to be upregulated in drug-resistant tumor cells, was shown to increase the apoptosis of cisplatin-resistant A549 cells following cisplatin treatment. Thus, our results provide an in-depth analysis of the signaling pathways that are commonly altered in drug-resistant NSCLC cell lines and highlight the potential strategy that facilitates the development of interventions to interfere with upregulated signaling pathways as well as to boost downregulated signaling pathways in drug-resistant tumors for the elimination of multiple resistance of NSCLC.
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Project description:Human non-transformed lung epithelial cell line (BEAS-2B) was transduced with a control (BEAS-C) or PI3KCA-E545K (BEAS-PI3K-CA) expressing lentivirus. After clones selection, RNA was extracted from three different clones for each cell line. For mRNA expression profiling, 500 ng total RNA were reverse transcribed and used for synthesis of cDNA and biotinylated cRNA. Finally cRNA were hybridized for 18 hours on Illumina HumanHT-12 v3.0 BeadChips and after scanning, data analysis was performed.
2012-03-01 | E-TABM-1192 | biostudies-arrayexpress
Project description:Non-small cell lung cancer (NSCLC) is a highly malignant type of cancer with a poor 5-year survival rate. The development of prognostic biomarkers and novel drug targets are required in order to improve the survival for NSCLC patients. Signal transducer and activator of transcription (STAT) proteins are cytoplasmic transcription factors known to play key roles in many cellular biological processes. However, the roles of STAT family members in the development and progression of NSCLC have not yet been apparently determined. Our study investigated the roles of STATs in the prognosis of NSCLC using cBioPortal, Human Protein Atlas, ONCOMINE, and Kaplan-Meier Plotter databases. High mutation rate of STATs existed in both lung adenocarcinoma (ADE) patients and squamous cell carcinoma (SCC) patients. High mRNA expression of STAT2 was significantly associated with shorter overall survival (OS) in NSCLC patients, while increased STAT5 and STAT6 were associated with better OS in NSCLC patients. We further found that increased mRNA expressions of STAT2 and STAT3 predicted unfavorable overall survival (OS) while high mRNA expression of STAT5B and STAT6 related to favorable OS for lung ADE patients. However, no significant correlation was identified for lung SCC patients. In stratified survival analysis, high expression of STAT2 predicted poor prognosis in stage II NSLCC patients, surgical margins negative patients and female patients. Taken together, our results illustrated that STAT5B and STAT6 could be effective prognostic biomarkers for survivals of NSCLC patients. And STAT2 might be a promising therapeutic target for the treatment of NSCLC as well as ADE.
| S-EPMC6731411 | biostudies-literature
Project description:Purpose Prospectively identifying who will benefit from adjuvant chemotherapy (ACT) would improve clinical decisions for individual non-small-cell lung cancer (NSCLC) patients. Most current molecular signatures for lung cancer are prognostic only and provide limited information with regard to the functional importance of the genes selected. In this study, we aim to develop and validate a functional gene set that predicts the clinical benefit of ACT in NSCLC. Experimental Design An 18-hub-gene prognosis signature was developed through a systems biology approach using a large NSCLC dataset from the Director’s Challenge Consortium. The prognostic value of this signature was tested in NSCLC patients from UT Lung SPORE cohort and additional five public datasets. The 18-hub-gene set was then integrated with genome-wide functional (RNAi) data and genetic aberration data to derive a 12-gene predictive signature for ACT benefit in NSCLC. Results We showed that the 18-hub-gene set can robustly predict the prognosis of patients with adenocarcinoma in all validation datasets across four microarray platforms. The refined 12-gene functional set was successfully validated in two independent datasets. The predicted benefit group showed significant improvement in survival after ACT (JBR.10 clinical trial data: hazard ratio=0.36, p=0.038; UT Lung SPORE data: hazard ratio=0.34, p=0.017), while the predicted non-benefit group showed no survival improvement. Conclusions This is the first study to integrate genetic aberration, genome-wide RNAi functional data, and mRNA expression data to identify a functional gene set that is predictive for ACT benefits. This 12-gene predictive signature has been validated in two independent NSCLC cohorts. Patients were eligible to enter the study if they underwent curative resection for NSCLC at MD Anderson Cancer Center between December 1996 and June 2007, and patients with radiation therapy were excluded from the study. All tissue samples were obtained by surgical resection from patients who had provided written informed consent. Tissues were stored at −140°C after being snap frozen in liquid nitrogen. Serial sectioning of each sample was used to histologically evaluate tumor and malignant cells content before RNA extraction. The primary tumor tissues from 176 patients were selected randomly from similar samples in the UT Lung SPORE tumor collection based on stringent, predefined quality control procedures before any data analysis, including the presence of ≥70% tumor tissue and ≥50% malignant cells in the frozen tissue used for RNA extraction. In this cohort, 133 patients are adenocarcinomas (ADCs) and 43 patients are squamous cell carcinomas (SCCs); 49 patients received ACT (mainly Carboplatin plus Taxanes) and 127 patients did not receive ACT.
| S-ECPF-GEOD-42127 | biostudies-other
Project description:Analysis of NSCLC development at gene expression level. Results shows that obvious activation of cell cycle pathway, and significant repression of cell-cell communication pathways. Illumina HumanHT-12 V4.0 expression beadchip Total RNA obtained from 6 paired NSCLC cancer tissue and the adjacent normal tissue.
| S-ECPF-GEOD-29249 | biostudies-other
Project description:Differences in gene expression profiles regarding the expression of genes encoding for proteins with G protein-coupled receptor (GPCR) activity between SCLC and NSCLC and normal lung samples was successfully examined. In the present study, 8 SCLC, 16 NSCLC and 14 normal lung RNA samples (human) had been purchased from OriGene Technologies. Gene expression analysis was performed using Affymetrix microarrays (Human Exon 1.0 ST Array).
| S-ECPF-GEOD-40275 | biostudies-other