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Expression data from Non small cell lung cancer cell lines

ABSTRACT: Non small cell lung cancer is the leading cause of cancer related mortality in the western world. RNA expression profiles have been demonstrated to be associated with a specific clinical course of the disease. We used microarray analysis to capture the whole transcriptome of a series of lung cancer cell lines to extract RNA profiles associated with specific genomic lesions Keywords: steady state

ORGANISM(S): Homo sapiens

PROVIDER: GSE14925 | GEO | 2009/04/15

SECONDARY ACCESSION(S): PRJNA111915

REPOSITORIES: GEO

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Expression data from Non small cell lung cancer cell lines

Project description:Non small cell lung cancer is the leading cause of cancer related mortality in the western world. RNA expression profiles have been demonstrated to be associated with a specific clinical course of the disease. We used microarray analysis to capture the whole transcriptome of a series of lung cancer cell lines to extract RNA profiles associated with specific genomic lesions Keywords: steady state Lung cancer cell lines were exponentially grown and harvested during this phase of exponential growth

2009-04-15 | E-GEOD-14925 | biostudies-arrayexpress

Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory mediators [452 expt: THP-1 vs BEAS 2B]

Project description:The goal of the study was to characterize gene expression profiles of lung epithelial and THP-1 monocytic cells influenzed by exposure to poultry dust extract. Gene expression profiles were determined by DNA microarrayanalysis using Illumina Human HT-12 v4 Expression bead chip, and changes in significantly induced transcripts validated by real time quantitative RT-PCR, ELISA, Western blotting and immunohistochemical staining. Significantly induced genes included IL-8, IL-6, ICAM-1, CCL2, CCL5, TLR4 and PTGS2. Pathway analysis indicated that dust extract treatment induced changes in gene expression influenced functions related to immune and inflammatory responses.

2015-09-16 | GSE73062 | GEO

Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory mediators [391 expt: A549 vs BEAS 2B]

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Mechanisms of drugs-resistance in small cell lung cancer

Project description:Lung cancer is the leading cause of cancer mortality and is classified by the World Health Organization into two broad histological subtypes. Non–small cell lung cancer (NSCLC), including adenocarcinoma, squamous cell carcinoma, and large cell carcinoma, accounts for ~85% of all lung cancer cases, with the remaining 15% of cases being due to small cell lung cancer (SCLC), which arises from neuroendocrine cells in the lung. Although most SCLC tumors are initially responsive to chemotherapy and radiation, patients often experience relapse, with the tumor acquiring an aggressiveness and therapeutic resistance that lead to a poor clinical outcome. Improvement of overall survival in individuals with SCLC will require the identification of novel therapeutic targets based on a better understanding of the changes in intracellular signaling of aggressive SCLC cells. The malignant progression of SCLC often occurs concomitantly with the acquisition of chemoresistance, suggesting that phenotypic malignant change is related to adaptation to the stresses induced by chemotherapy. In order to analyze gene expression changes associated with malignant transformation in SCLC, we established a cisplatin-resistant SCLC cell line and performed RNA sequencing.

2021-03-04 | GSE168184 | GEO

Global Methylation Patterns in Idiopathic Pulmonary Fibrosis

Project description:Idiopathic Pulmonary Fibrosis (IPF) is a chronic progressive lung disease that affects more than 5 million people worldwide with a steady increase in both incidence and mortality. There is currently no effective therapy and the median survival without transplant is 2-5 years. The etiological factor is unknown, but several observational and pathogenesis studies suggest that environmental agents may cause IPF. DNA methylation is a type of chemical modification of DNA such environmental and occupational factors, that can induced a changes in the regulation of biological processes and link to diseases such as a cancer. We hypothesize that the global changes in methylation patterns of IPF lungs caused by environmental factors. In this study we will identify the global methylation signatures of the IPF lung and to compare to methylation signature of lung cancer. The DNA methylation profiles of IPF lung tissue differs from control lung but it shares great similarity with that of lung cancer.

2012-04-19 | GSE29895 | GEO

Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory mediators [391 expt: A549 vs BEAS 2B]

2015-09-16 | E-GEOD-73061 | biostudies-arrayexpress

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2015-09-16 | E-GEOD-73062 | biostudies-arrayexpress

LCMR1 Promotes Large-cell Lung Cancer Proliferation and Metastasis through Downregulation of HLA Coding Genes

Project description:Lung cancer is notorious for high morbidity and mortality around the world. We previously cloned the gene LCRM1 from human large-cell lung carcinoma cell line, however whether this gene affect the proliferation and metastasis of large-cell lung carcinoma is yet unknown. To fully identify the biofunction of LCMR1 in lung cancer, we performed pan-cancer and cell line based LCMR1 expression profiling. Our analysis indicated that LCMR1 was expressed at higher levels in most solid tumors, especially in NSCLC. The expression profile of LCMR1 in different NSCLC cell lines revealed the highest level in the large-cell lung cancer cell 95D. Furthermore, our functional studies using lentivirus-based knockdown strategies indicates that LCMR1 is critical for large-cell lung cancer proliferation, migration, and invasion in cultured cells, and blocking this gene significantly reduced the growth of 95D cell xenograft mouse model. In mechanism assay, multiple sequence-based assay revealed that LCMR1 diminished the RNA Pol II occupancy at the promoter of HLA coding genes, thus blocks the transcription of these genes. Also, the correlation assay of TCGA database suggested that the expression level of LCMR1 was negatively related with the HLA coding genes, which plays vital role in cancer-specific antigen presenting and anticancer immunity. In conclusion, our studies showed that LCMR1 is required for large-cell lung cancer cell growth and invasion, suggesting its potential as a valid target in clinical treatment.

2023-08-01 | GSE234816 | GEO

Proteome of silenced minichromosome maintenance protein 2 with siRNA on non-small cell lung cancer H1299 cells

Project description:Lung cancer is the leading cause of cancer-related mortality. The two main lung cancer types are small cell lung cancer (SCLC) and non-SCLC (NSCLC), where NSCLC comprises about 80-85% of all lung cancer. Despite the introduction of improved treatments, the overall survival rate of lung cancer patients remains low. Further elucidation of the regulatory network perturbations between cancer-related genes and proteins is one promising route to alter this mortality trend. The deregulation of the DNA replication, cell cycle, proliferation and migration are the common factors that are involved in cancer development and progression, and therefore logical targets for analysis. Minichromosome maintenance 2(MCM2) is a DNA replication licensing factor, which belongs to the heterohexameric MCM2-7 complex. MCM2 has been proposed as an excellent proliferation marker in many types of cancer. Our study will establish a global functional distribution of identified proteins in silenced-MCM2 in H1299 NSCLC by the means of iTRAQ. Understanding the molecular basis of MCM2 in lung cancer cells enables us to discover alternative target for lung cancer therapy.

2018-10-26 | PXD003743 | Pride

Single cell RNA sequencing analysis of freshly resected non-small cell lung carcinoma (NSCLC) tissues

Project description:Lung cancer is the leading cause of cancer-related deaths world-wide. ~85% of lung carcinomas are non–small cell lung carcinoma (NSCLC). Tumor cell heterogeneity is very poorly defined. However, it is known to be important for tumor response to cancer therapy and cancer agressivenes. We subjected three NSCLC tumors resected from different patients to Drop-seq in order to 1) elucidate the capability of scRNA-seq analysis in identifying different tumor cell populations; and 2) ascertain the clinical value of the genes which distinguish cancer cells from other cells in the tissue. As anticipated, the tissue composition of independently collected samples varied. Despite deficient populations in some samples, both donor and patient samples contributed to the majority of cell populations. However, cancer cells were all patient-specific. These findings emphasize the utility of single cell gene expression data in identification of tumor cell populations. The collected data might be further used for predicting of drugs specific to the biology of activated pathways and patient outcome.

2020-12-19 | GSE148466 | GEO

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