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Homo sapiens

ABSTRACT: Transcriptional profiles of TIMP-2 and Ala+TIMP-2 A549 overexpressing cells and in tumor xenografts.

OTHER RELATED OMICS DATASETS IN: E-GEOD-38408

PROVIDER: PRJNA167800 | ENA |

REPOSITORIES: ENA

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E-GEOD-38408

Project description:Transcriptional profiles of TIMP-2 and Ala+TIMP-2 A549 overexpressing cells and in tumor xenografts.

2015-08-19 | E-GEOD-38408 | ExpressionAtlas

Transcriptional profiles of TIMP-2 and Ala+TIMP-2 A549 overexpressing cells and in tumor xenografts.

Project description:TIMP-2 is an endogenous angiogenesis inhibitor, i.e. inhibits endothelial cell proliferation and tumor angiogenesis. As a result, TIMP-2 inhibits tumor growth and progression to metastasis. Understanding, therefore, the mechanisms of TIMP-2-mediated tumor growth inhibition would provide further support on the use of TIMP-2 as a novel biological agent for cancer therapy. We used microarray analysis to determine the TIMP-2 and Ala+TIMP-2 transcriptional profiles of A549 cancer cells in order to understand how TIMP-2 inhibits tumor growth and angiogenesis. We overexpressed TIMP-2 and its mutant (does not inhibit MMP) in A549 human lung cancer cells and determined TIMP-2 and Ala+TIMP-2 transcriptional profiles, groups of genes and associated biological functions. We then injected the cells in NOD-SCID mice and RNA from tumors were isolated for further analysis to identify genes that are associated with tumor growth inhibition.

2013-01-28 | E-GEOD-38408 | biostudies-arrayexpress

Transcriptional profiles of TIMP-2 and Ala+TIMP-2 A549 overexpressing cells and in tumor xenografts.

2013-01-28 | GSE38408 | GEO

Transcription profiling of human A549 lung cancer cells and their isogenic mitochondrial DNA (mtDNA)-depleted rho zero counterparts grown in cell culture and as tumor xenografts in immune-deficient mice.

Project description:Interactions between the gene products encoded by the mitochondrial and nuclear genomes play critical roles in normal eukaryotic cellular function. Here, we characterized the metabolic and transcriptional properties of A549 lung cancer cells and their isogenic mitochondrial DNA (mtDNA)-depleted rho zero counterparts grown in cell culture and as tumor xenografts in immune-deficient mice. A manuscript summarizing our conclusions is under review. Experiment Overall Design: A549 rho zero and their parental A549 cells were grown in culture and as xenografts in nude mice. All experiments conducted in culture were performed in triplicate (6 experiments total) and all experiments conducted in xenografts were performed in quadruplicate (8 experiments total). A manuscript summarizing our experimental design is under review.

2008-06-11 | E-GEOD-10957 | biostudies-arrayexpress

Expression data from miR340 overexpressing human A549 cells

Project description:To characterize the differentially expressed genes of miR340, we compared the gene expression profiles of miR-340 overexpressing human A549 cells with that of empty vector transfected A549 cells

2019-01-01 | GSE115361 | GEO

Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer [miRNA]

Project description:This experiment is designed to screen miRNAs that are deregulated during chemoresistance-associated metastasis of lung cancer cells. Chemoresistant metastatic in vivo tumor model of A549-luc-Vector cells was established after four rounds of cisplatin (CDDP) treatments compared to corresponding control solvent treatments. Upon examining profiles of miRNA expression differential between tumor-derived cultured cells from the Ctrl-4th and CDDP-4th treatments, most markedly upregulated and downregulated miRNAs in chemoresistant, metastatic A549-luc-CDDP-4th cells were identified. In order to establish a chemoresistant in vivo tumor model, after inoculation of A549-luc-Vector cells, cisplatin (CDDP) or control solvent was intraperitoneally (i.p.) injected six rounds in a two-week period and cells were isolated from corresponding resultant tumors, cultured and re-transplanted into syngeneic mice to receive the next round of treatment. In our experimental model, human lung cancer xenografts developed chemoresistance in the third round of CDDP treatment (CDDP-3rd) and chemoresistance-associated metastases following the fourth round of treatment. Tumor-derived cultured cells from Ctrl-4th and CDDP (cisplatin)-4th treatment were subjected to miRNA array (Agilent-031181 human miRNA (8*60k) V16.0) analysis, with two biological replications for each treatment.

2015-04-10 | E-GEOD-67727 | biostudies-arrayexpress

Single-cell analysis reveals dynamic changes of A549 cells in monolayer, A549 xenografts in nude mice, and xenografts after exposure to dacomitinib

Project description:The in vitro A549 cells, and A549 xenografts in nude mouse were two classic and commonly used models for anti-cancer drug discovery. Here dynamic changes of the A549 models, and also A549 xenografts after exposure to dacomitinib were revealed by single-cell transcriptome analysis.

2023-12-01 | GSE220435 | GEO

Profiling protease and protease inhibitor gene expression in tumors and their microenvironment

Project description:To assist in the identification of proteases, their endogenous inhibitors, and proteins that interact with proteases or proteolytic pathways in biological tissues, a dual species oligonucleotide microarray has been developed in conjunction with Affymetrix, Inc. To investigate the performance of the array, gene expression profiles were analyzed in pure mouse and human samples and orthotopically implanted xenografts of human A549 lung and MDA-MB-231 breast carcinomas. The Hu/Mu ProtIn array is a valuable discovery tool for the identification of components of human and murine proteolytic pathways in health and disease, and has particular utility in the determination of cellular origins of proteases and protease inhibitors in xenograft models of human cancer. Keywords: gene expression profiles were analyzed in pure mouse and human samples and orthotopically implanted xenografts of human A549 lung and MDA-MB-231 breast carcinomas Commercial pan human and mouse total RNA replicate samples (n=3) were profiled. In addition, human ductal stage II or III breast carcinoma biopsies (n=18) were compared to normal human breast biopsies (n=13). Spontaneous spontaneous murine mammary carcinomas from MMTV-PyMT+(FVB/n) (n=8) and MMTV-PyMT+/uPARAP-/-(FVB/n) (n=2) transgenic mice were compared to normal mouse mammary fat pads (n=4; female Rag-1 tm1Mom retired breeders at >6 weeks post lactation). In vitro cultures of MDA-MB-231 human breast carcinoma cells (n=3) and MDA-MB-231 orthotopic xenografts (n=3) were profiled. The xenografts were compared to normal mammary fat pads. A549 human lung adenocarcinoma cells (n=2), A549 orthotopic xenografts (n=3) and normal mouse lung tissue (n = 3) were profiled.

2008-07-20 | E-GEOD-6413 | biostudies-arrayexpress

RNA-seq of human lung cancer cell line A549-NC and A549-SLC2A5 knockout xenograft in balb/c nude mice.

Project description:We deleted SLC2A5 using CRISPR-Cas9 technology in human lung cancer cell A549. Control A549 cells and A549 cells with SLC2A5 knockout were transplanted in balb/c nude mice. Then RNA-seq was performed in control A549 and SLC2A5 ablation A549 Xenografts.

2019-12-12 | E-MTAB-8572 | biostudies-arrayexpress

Expression data from discodermolide sensitive and resistant cell lines

Project description:Discodermolide treatment of A549 results in senescence. We compared cells resistant to disco-induced senescence to those that are sensitive to senescence induction. We also examined the gene expression of resistant (AD32) cells overexpressing 4E-BP1, a protein known to restore sensitivity to discodermolide in these cells. Total RNA was collected from A549, A549 disco, AD32, and AD32 4E-BP1 cells and gene expression profiles were examined.

2010-12-08 | E-GEOD-25904 | biostudies-arrayexpress

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