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MicroRNA expression data from high and low invasive A549 human lung adenocarcinoma cells

ABSTRACT: The major cause of cancer-related deaths in lung cancer patients is commonly attributed to its ability to metastasize to distant organs such as the bone, brain, liver and adrenal glands. The dysregulation in miRNA expression is believed to contribute toward the initiation and progression of metastasis through their capability to regulate target genes. In this study, two NSCLC sub-cell lines possessing opposing migration and invasion properties were established using serial transwell invasion assays, followed by miRNA microarray to obtain the overview of miRNA expression as well as identify important playes in metastasis. High and low invasive A549 sub-cell lines were established from heterogeneous parental population and selected through seven generations. Three replicates were used for RNA extraction and miRNA microarray.

ORGANISM(S): Homo sapiens

SUBMITTER: san ho

PROVIDER: S-ECPF-GEOD-47056 | biostudies-other |

REPOSITORIES: biostudies-other

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MicroRNA expression data from high and low invasive A549 human lung adenocarcinoma cells

Project description:The major cause of cancer-related deaths in lung cancer patients is commonly attributed to its ability to metastasize to distant organs such as the bone, brain, liver and adrenal glands. The dysregulation in miRNA expression is believed to contribute toward the initiation and progression of metastasis through their capability to regulate target genes. In this study, two NSCLC sub-cell lines possessing opposing migration and invasion properties were established using serial transwell invasion assays, followed by miRNA microarray to obtain the overview of miRNA expression as well as identify important playes in metastasis.

2013-12-08 | GSE47056 | GEO

MicroRNA expression data from high and low invasive A549 human lung adenocarcinoma cells

2013-12-08 | E-GEOD-47056 | biostudies-arrayexpress

MicroRNA expression data from Bcl-xL silenced A549 lung adenocarcinoma cells

Project description:Bcl-xL is an anti-apoptotic protein that is frequently found to be overexpressed in non-small cell lung cancer leading to an inhibition of apoptosis and poor prognosis. Recently, the role of miRNAs in regulating apoptosis and cell survival during tumorigenesis has become evident, with cancer cells showing perturbed expression of various miRNAs. We utilized miRNA microarrays to determine if miRNA dysregulation in bcl-xL silenced lung adenocarcinoma cells could be involved in regulating apoptotic behavior, and identified dysregulated miRNAs with putative targets involved in signal transduction pathways regulating apoptosis, cell proliferation and cell progression. Short interfering RNA-based transfection of A549 was carried out inducing a reduction in bcl-xL expression levels. 24 hours post-transfection total RNA was isolated using TRIzol reagent and hybridized onto Affymetrix GeneChip miRNA Arrays. A global miRNA expression profile was then established, which compared total RNA, extracted from siRNA-transfected and non-transfected A549 cells. All experiments were carried out with three independent biological replicates.

| S-ECPF-GEOD-47059 | biostudies-other

MicroRNA expression data from Bcl-xL silenced A549 lung adenocarcinoma cells

2013-05-18 | GSE47059 | GEO

BRM270 inhibits cancer stem cell maintenance via microRNA regulation in chemoresistant A549 lung adenocarcinoma cells.

Project description:Chemotherapy is a standard treatment for non-small-cell lung cancer (NSCLC). However, the dose-limiting toxicity of drugs and the development of chemoresistance are major clinical challenges to successful management of NSCLC. Asian traditional medicine is gaining global attention as a non-toxic alternative to chemotherapy. BRM270 is an extract formulated from seven Asian medicinal plants that has been shown to inhibit tumor cell proliferation in diverse cancer types. We previously demonstrated that BRM270 suppresses tumorigenesis by negatively regulating nuclear factor-κB signaling in multidrug-resistant cancer stem cells (CSCs). In this study we report that the growth, migration, and invasion of normal human lung adenocarcinoma cells and their chemoresistant derivatives was inhibited by BRM270 treatment. Notably, BRM270 was found to modulate CSC self-renewal and tumor-initiating capacity via positive regulation of the miRNA-128. Thus, combination therapy with miRNA-128 and BRM270 may be an effective treatment strategy for chemoresistant NSCLC.

| S-EPMC5833813 | biostudies-literature

Quercetin Decreases Claudin-2 Expression Mediated by Up-Regulation of microRNA miR-16 in Lung Adenocarcinoma A549 Cells.

Project description:Claudin-2 is highly expressed in human lung adenocarcinoma tissues and cells. Knockdown of claudin-2 decreases cell proliferation and migration. Claudin-2 may be a novel target for lung adenocarcinoma. However, there are no physiologically active substances of foods which decrease claudin-2 expression. We here found that quercetin, a flavonoid present in fruits and vegetables, time- and concentration-dependently decreases claudin-2 expression in lung adenocarcinoma A549 cells. In the present study, we examined what regulatory mechanism is involved in the decrease in claudin-2 expression by quercetin. Claudin-2 expression was decreased by LY-294002, a phosphatidylinositol 3-kinase (PI3-K) inhibitor, and U0126, a MEK inhibitor. These drugs inhibited the phosphorylation of Akt and ERK1/2, which are downstream targets of PI3-K and MEK, respectively. In contrast, quercetin did not inhibit the phosphorylation. Both LY-294002 and U0126 inhibited promoter activity of claudin-2, but quercetin did not. The stability of claudin-2 mRNA was decreased by quercetin. Quercetin increased the expression of microRNA miR-16. An inhibitor of miR-16 rescued quercetin-induced decrease in the claudin-2 expression. These results suggest that quercetin decreases claudin-2 expression mediated by up-regulation of miR-16 expression and instability of claudin-2 mRNA in lung adenocarcinoma cells.

| S-EPMC4488803 | biostudies-other

expression data from human lung adenocarcinoma cells A549

Project description:expression data from human lung adenocarcinoma cells A549

| PRJNA411770 | ENA

MicroRNA expression data from Bcl-xL silenced A549 lung adenocarcinoma cells

2013-05-18 | E-GEOD-47059 | biostudies-arrayexpress

Gene expression profiling of cancer stem cell in human lung adenocarcinoma A549 cells.

Project description:BackgroundThe studies on cancer-stem-cells (CSCs) have attracted so much attention in recent years as possible therapeutic implications. This study was carried out to investigate the gene expression profile of CSCs in human lung adenocarcinoma A549 cells.ResultsWe isolated CSCs from A549 cell line of which side population (SP) phenotype revealed several stem cell properties. After staining the cell line with Hoechst 33342 dye, the SP and non-side population (non-SP) cells were sorted using flow cytometric analysis. The mRNA expression profiles were measured using an Affymetrix GeneChip(R) oligonucleotide array. Among the sixty one differentially expressed genes, the twelve genes inclusive three poor prognostic genes; Aldo-keto reductase family 1, member C1/C2 (AKR1C1/C2), Transmembrane 4 L six family member 1 nuclear receptor (TM4SF1), and Nuclear receptor subfamily 0, group B, member 1 (NR0B1) were significantly up-regulated in SP compared to non-SP cells.ConclusionThis is the first report indicating the differences of gene expression pattern between SP and non-SP cells in A549 cells. We suggest that the up-regulations of the genes AKR1C1/C2, TM4SF1 and NR0B1 in SP of human adenocarcinoma A549 cells could be a target of poor prognosis in anti-cancer therapy.

| S-EPMC2234429 | biostudies-literature

expression data from human lung adenocarcinoma cells A549

Project description:GMDS is important for human lung adenocarcinoma progression, detailed molecular mechanisms remain elusive. We used microarray to detail the global gene expression changes in A549 cells with GMDS knockdown as compared to control cells

2017-12-24 | GSE104123 | GEO

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