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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse sarcoma cell lines CMS4 vs. CMS4-met

ABSTRACT: To identify unique genes associated with tumor progression by comparing a poorly metastatic tumor cell line with a highly metastatic tumor cell line.

ORGANISM(S): Mus musculus

SUBMITTER: Sheila Caldwell

PROVIDER: E-MEXP-277 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Cooperative disengagement of Fas and intercellular adhesion molecule-1 function in neoplastic cells confers enhanced colonization efficiency.

Liu Kebin K Caldwell Sheila A SA Abrams Scott I SI

Cancer research 20050201 3

Understanding the mechanisms of tumor progression is crucial toward the development of therapeutic interventions. Although the loss of sensitivity to cell death is a hallmark of neoplastic progression, it is likely one of several essential features that underlie a malignantly proficient or aggressive tumorigenic phenotype. Here, we identified intercellular adhesion molecule-1 (ICAM-1) as a molecule with expression coordinately regulated with Fas and inversely correlated with malignant phenotype ...[more]

PMID: 15705906

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Transcription profiling of in vivo-derived CMS4-met cells and the in vitro-derived CMS4.sel cells using CMS4 cells as a reference sample

Project description:The CMS4 sarcoma, kindly provided by A. DeLeo (University of Pittsburgh, Pittsburgh, PA), is a solid tumor of BALB/c (H-2d) origin, which grows aggressively in naive, syngeneic hosts following a s.c. transplant. Although the parental tumor cell line forms few metastatic foci in the lungs following i.v. administration, a highly metastatic subline, termed CMS4-met, was established from lung digests of those mice as described (Ryan MH, Bristol JA, McDuffie E, Abrams SI. Regression of extensive pulmonary metastases in mice by adoptive transfer of antigen-specific CD8(+) CTL reactive against tumor cells expressing a naturally occurring rejection epitope. J Immunol 2001;167:4286-92). The CMS4.sel subline was selected from the parental line in vitro following six successive passages in the presence of anti-Fas stimuli as described (Liu K, Abrams SI. Alterations in Fas expression are characteristic of, but not solely responsible for, enhanced metastatic competence. J Immunol 2003;170:5973-80).<br>In this experiment we compare the gene expression patterns of the in vivo-derived CMS4-met cells and the in vitro-derived CMS4.sel cells using CMS4 cells as a reference sample.

2005-05-08 | E-MEXP-286 | biostudies-arrayexpress

Transcription profiling of mouse control cell line and a cell line surviving exposure to tumor-specific CTL (cytolytic T lymphocyte)

Project description:The CMS4 sarcoma, kindly provided by A. DeLeo (University of Pittsburgh, Pittsburgh, PA), is a solid tumor of BALB/c (H-2d) origin, which grows aggressively in naive, syngeneic hosts following a s.c. transplant. Although the parental tumor cell line forms few metastatic foci in the lungs following i.v. administration, a highly metastatic subline, termed CMS4-met, was established from lung digests of those mice as described (Ryan MH, Bristol JA, McDuffie E, Abrams SI. Regression of extensive pulmonary metastases in mice by adoptive transfer of antigen-specific CD8(+) CTL reactive against tumor cells expressing a naturally occurring rejection epitope. J Immunol 2001;167:4286-92).<br>In this experiment we compare the gene expression profiles between a control cell line and a cell line surviving exposure to tumor-specific CTL (cytolytic T lymphocyte). CMS4-met cells were injected iv. to the mouse tails. Three days later, either saline or tumor-specific CTL were injected iv into mouse tails. Single cell suspensions were made from mouse lungs and put in culture. Tumor cells were recovered from cultures. Tumor cells established from mice receiving saline were termed CMS4-met.cntl. Tumor cells established from mice receiving CTL were termed CMS4-met.sel. The gene expression profiles of these two tumor cell lines were then compared to CMS4-met.

2005-05-08 | E-MEXP-287 | biostudies-arrayexpress

Transcription profiling of mouse CMS4 and CMS4-met cell lines after IFNgamma treatment

Project description:The CMS4 sarcoma, kindly provided by A. DeLeo (University of Pittsburgh, Pittsburgh, PA), is a solid tumor of BALB/c (H-2d) origin, which grows aggressively in naive, syngeneic hosts following a s.c. transplant. Although the parental tumor cell line forms few metastatic foci in the lungs following i.v. administration, a highly metastatic subline, termed CMS4-met, was established from lung digests of those mice as described (Ryan MH, Bristol JA, McDuffie E, Abrams SI. Regression of extensive pulmonary metastases in mice by adoptive transfer of antigen-specific CD8(+) CTL reactive against tumor cells expressing a naturally occurring rejection epitope. J Immunol 2001;167:4286-92).<br>In this experiment we compare gene expression kinetics in the CMS4 and CMS4-met cell lines after IFNgamma treatment. Both cells were treated with IFNgamma for 4 and 24 hours respectively. The untreated and treated cells were then used for total RNA isolation, and microarray experiments.

2005-05-08 | E-MEXP-288 | biostudies-arrayexpress

SCGB3A2 suppresses bleomycin-induced pulmonary fibrosis through activation of STAT1 and up-regulation of SMAD7

Project description:We report for the first time that secretoglobin (SCGB) 3A2, a novel cytokine-like molecule, predominantly expressed in pulmonary airways epithelium, drastically reduced the severity of lung fibrosis using bleomycin-induced mouse model. DNA microarrays were performed using RNAs isolated from mouse lungs in two experiments. In the first experiments, mice were adminitered intravenously SCGB3A2 or PBS once daily for a week, starting on day 14 after BLM administration, and in the second experiments, SCGB3A2 or PBS was administered intravenously for 12 hrs.

2011-04-30 | E-GEOD-21560 | biostudies-arrayexpress

Isolation and expression profiling of circulating tumor cells in breast cancer patients part 1

Project description:We developed a method to isolate pure circulating tumor cells (CTC). RNA from such CTCs isolated from the peripheral blood of metastatic breast cancer patients and gene expression was performed using cDNAmicroarray. we used cDNA array to compare gene expression of CTCs with normal epithelial and breast tumor samples normal blood vs. breast tumor

2014-12-18 | E-GEOD-45962 | biostudies-arrayexpress

Isolation and expression profiling of circulating tumor cells in breast cancer patients part 3

Project description:We developed a method to isolate pure circulating tumor cells (CTC). RNA from such CTCs isolated from the peripheral blood of metastatic breats cnacer patients and gene expression was performed using cDNAmicroarray. we used cDNA array to compare gene expression of CTCs with normal epithelial and breast tumor samples CTCs vs. breast tumors

2014-12-18 | E-GEOD-45964 | biostudies-arrayexpress

Isolation and expression profiling of circulating tumor cells in breast cancer patients part 2

2014-12-18 | E-GEOD-45963 | biostudies-arrayexpress

An Ets2-specific transcriptional program in tumor-associated macrophages promotes metastasis

Project description:Macrophages have been implicated in breast cancer progression and metastasis, but relatively little is known about the genes and pathways that are involved. Using a conditional allele of Ets2 in the mouse, we have identified Ets2 as a critical gene in tumor associated macrophages (TAMs) that specifically promotes mammary tumor metastasis. Loss of Ets2 in TAMs decreased the frequency and size of lung metastases without impacting primary tumor burden. Expression profiling of isolated tumor macrophages established that Ets2 deficiency resulted in the de-repression of a defined set of anti-angiogenic genes. Activation of this transcriptional program correlated with decreased angiogenesis in metastatic tumors and decreased metastatic growth. Comparison of this Ets2-specific TAM expression profile with human breast cancer profiles revealed a macrophage gene expression signature that could predict overall survival of estrogen receptor negative patients. In summary, we have identified a critical factor, Ets2, in TAMs that represses a transcriptional program to promote the growth of mammary tumor metastases in the lung. Breast TAMs were isolated from early-stage PyMT-induced mammary tumors expressing Ets2 and also from the tumors with Ets2-deficient TAMs. Since macrophages have also been implicated in normal mammary gland remodeling, normal remeodeling macrophages were also purified from females expressing Ets2 and the ones where Ets2 is deleted in the macrophages. One RNA sample was extracted from each genetic group for gene-expression profiling.

2010-01-05 | E-GEOD-12863 | biostudies-arrayexpress

High Mobility Group protein HMGB2 is a Critical Regulator of Plasmodium Oocyst Development

Project description:Two mice per group were infected with one million purified schizonts from the WT and two clones (B3 and D1) of the pyhmgb2 KO lines. Parasitemia reached 10 to 20 % and equivalent gametocytemia total RNA was extracted from the WT and the B3 and D1 clones of the KO parasite lines using the Trizol method on saponin lysed of parasites. Four samples analysed including dye-swap

2008-04-19 | E-GEOD-9952 | biostudies-arrayexpress

Role for ISGF3II in the Antiviral Activity of IFN-gamma

Project description:Type-I (e.g. IFN-alpha, IFN-beta) and type-II IFNs (IFN-gamma) have antiviral, antiproliferative, and immunomodulatory properties. Both types of IFN signal through the Jak/STAT pathway to elicit antiviral activity, yet IFN-gamma is thought to do so only through STAT1 homodimers while type-I IFNs activate both STAT1- and STAT2-containing complexes such as ISGF3. Here we show that ISGF3II - composed of phosphorylated STAT1, unphosphorylated STAT2, and IRF9 - also plays a role in IFN-gamma-mediated antiviral activity in humans. Using phosphorylated STAT1 as a marker for IFN signaling, western blot analysis of IFN-alpha2a treated human A549 cells revealed that pSTAT1 (Y701) levels peaked at 1h, decreased by 6h, and remained at low levels for up to 48h. Cells treated with IFN-gamma showed a biphasic pSTAT1 response with an early peak at 1-2h and a second peak at 15-24h. Gene expression microarray following IFN-gamma treatment for 24h indicated an induction of antiviral genes that are induced by ISGF3 and associated with a type-1 IFN response. Induction of these genes by autocrine type-I and type-III IFN signaling was ruled out using neutralizing antibodies to these IFNs in biological assays and by qRT-PCR. Despite the absence of autocrine IFNs, IFN-gamma treatment induced formation of ISGF3II. This novel transcription factor complex binds to ISRE promoter sequences, as shown by ChIP analysis of the PKR promoter. STAT2 and IRF9 knockdown in A549 cells reversed IFN-gamma-mediated ISRE induction and antiviral activity - implicating ISGF3II formation as a significant component of the cellular response and biological activity of IFN-gamma. Two treatments using three biological replicates each were performed using three million A549 cells. Each was seeded overnight in 10mL complete RPMI and treated. Three were treated with alpha-IFN and three treated with gamma-IFN for 24h. Control samples were left untreated.

2011-01-19 | E-GEOD-25113 | biostudies-arrayexpress

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