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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.

ORGANISM(S): synthetic construct Homo sapiens

PROVIDER: GSE47056 | GEO | 2013/12/08

SECONDARY ACCESSION(S): PRJNA203381

REPOSITORIES: GEO

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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. 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.

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

lncRNA/mRNA expression profiling of miR-200c-overexpressing MDA-MB-231 cells

Project description:MiR-200c is a well-studied miRNA that is involved in stemness, the epithelial-mesenchymal transition, chemoresistance, radioresistance, and invasion/metastasis of various cancer cells. To obtain an overview of the lncRNA/mRNA regulated by miR-200c signaling in breast-cancer cell lines, we performed global lncRNA/mRNA-expression profiling on MDA-MB-231-pGIPZ and MDA-MB-231-miR-200c cells.

2018-08-28 | GSE119090 | GEO

KLF17 is a negative regulator of epithelial-mesenchymal transition and metastasis in breast cancer

Project description:Metastasis is a complex multi-step process requiring the concerted action of many genes and is the primary cause of cancer deaths. Pathways that regulate metastasis enhancement and suppression both contribute to tumor dissemination process. In order to identify novel metastasis suppressors, we set up a forward genetic screen in a mouse model. We transduced a genome-wide RNAi library into the non-metastatic 168FARN breast cancer cell line, orthotopically transplanted the cells into mouse mammary fat pads, and then selected for cells that could metastasize to the lung and identified an RNAi for the KLF17 gene. Conversely, ectopic expression of KLF17 in highly metastatic 4T1 breast cancer cell line inhibited their ability to metastasize from the mammary fat pad to the lung. We showed that suppression of KLF17 expression promotes breast cancer cell invasion and epithelial-mesenchymal transition (EMT). We also showed that KLF17 functions by directly binding to the promoter of Id-1, a key metastasis regulator in breast cancer, to inhibit its transcription. Finally, we demonstrated that KLF17 expression is significantly down-regulated in primary human breast cancer samples and that the combined expression patterns of KLF17 and Id-1 can serve as a potential biomarker for lymph node metastasis in breast cancer.

2009-11-30 | GSE17081 | GEO

HSC-3 cells (control) vs. HSC-3-5 cells [cell line]

Project description:HSC-3-5 cells were derived from human HSC-3 cells via transwell invasion assay. Transcriptional profiling of human HSC-3 cells comparing with high invasive HSC-3-5 cells. Goal was to determine the effects of invasion on global HSC-3-5 gene expression during tumor metastasis. Two-condition experiment, HSC-3 vs. HSC-3-5 cells.

2013-08-13 | E-GEOD-39723 | biostudies-arrayexpress

HSC-3 cells (control) vs. HSC-3-5 cells [cell line]

2013-08-13 | GSE39723 | GEO

HSC-3 cells (control) vs. HSC-3-5 cells [subcutaneous tumor]

Project description:HSC-3-5 cells, which drived from human HSC-3 cells via transwell invasion assay was high invasive.Tumor cells were injected into the flank of SCID mice. After 6 weeks, transcriptional profiling of human HSC-3 tumor comparing with high invasive HSC-3-5 tumor. Goal was to determine the effects of invasion on global HSC-3-5 gene expression during tumor metastasis.

2013-08-13 | GSE39726 | GEO

HSC-3 cells (control) vs. HSC-3-5 cells [tongue]

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MicroRNAs among esophageal cancer cell sublines with different migration ability

Project description:Cellular directed migration is critical to invasion-metastasis cascade of cancer cells. We used in vitro transwell model to screen two esophageal cancer cell lines (KYSE30/180) and obtained two pairs of subpopulations with distinc motiliyt ability. Then we used microarrays to detail the differentially expressed genes and microRNAs between these two cell sublines (30U/D and 180U/D) to identify those responsible for ESCC motility. KYSE30/180 cells were subject to four successive selections using transwell (CORNING, USA). Subpopulations penetrated through membrane (D) or not (U) were harvested respectively for RNA extraction and hybridization on Affymetrix genome and LC Sciences microRNA microarrays

2015-12-31 | E-GEOD-67509 | biostudies-arrayexpress

HSC-3 cells (control) vs. HSC-3-5 cells [tongue]

Project description:HSC-3-5 cells, which drived from human HSC-3 cells via transwell invasion assay was high invasive.Tumor cells were injected into the tongue of SCID mice. After 1 week, transcriptional profiling of human HSC-3 tumor comparing with high invasive HSC-3-5 tumor. Goal was to determine the effects of invasion on global HSC-3-5 gene expression during tumor metastasis. HSC-3 and HSC-3-5 oral cancer cells were respectively injected into the tongue of SCID mice. After 1 weeks, total RNA was respectively extracted from the tumor tissue on tongue of SCID mice for gene expression profiling during metastasis. Briefly, two-condition experiment,HSC-3 vs. HSC-3-5 cells.

2013-08-13 | E-GEOD-39725 | biostudies-arrayexpress

B-catenin downregulates Dicer to promote ovarian cancer metastasis

Project description:Ovarian cancer is a nearly uniform lethal disease and its highly aggressive metastatic phenotype portends a poor prognosis. Lack of a well-controlled, relevant experimental model has been a major obstacle to identifying key molecules causing metastasis. Here we describe the creation of a new isogenic model of spontaneous human ovarian cancer metastasis exhibiting opposite phenotypes - highly metastatic (HM) and non-metastatic (NM) - both in vitro and in vivo. HM was unique in its ability to metastasize consistently to the peritoneum, mimicking the major dissemination route of human ovarian cancer. In contrast, NM failed to form detectable metastases although it was equally tumorigenic. Using comparative label-free quantitative LC-MS/MS, we identified b-catenin which we demonstrated for the first time a direct role in the pathogenesis of ovarian cancer metastasis. Our studies also revealed a previously unrecognized role of b-catenin in the downregulation of multiple microRNAs (miRNAs) through attenuating miRNA biogenesis by targeting Dicer, a key component of the microRNA processing machinery. One such downregulated miRNAs was miR-29s involved in epithelial-to-mesenchymal transition and subsequent stem cell traits. Silencing b-catenin or overexpressing Dicer or miR-29 mimics in HM significantly reduced the ability of these cells to migrate. B-catenin knockdown cells also failed to metastasize in an orthotopic model of ovarian cancer. Meta-analysis revealed an increase in CTNNB1 and a decrease in DICER1 expression levels in the high-risk group. These results uncover b-catenin as a critical player in promoting ovarian cancer aggressiveness and a new mechanism linking between b-catenin and miRNA downregulation underlying this process.

2017-07-03 | PXD006327 | Pride

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