Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE15181
PROVIDER: PRJNA114989 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cultured cancer cells exhibit substantial phenotypic heterogeneity when measured in a variety of ways such as sensitivity to drugs or the capacity to grow under various conditions. Among these, the ability to exhibit anchorage-independent cell growth (colony forming capacity in semisolid media) has been considered to be fundamental in cancer biology because it has been connected with tumor cell aggressiveness in vivo such as tumorigenic and metastatic potentials, and also utilized as a marker for in vitro transformation. Although multiple genetic factors for anchorage-independence have been identified, the molecular basis for this capacity is still largely unknown. To investigate the molecular mechanisms underlying anchorage-independent cell growth, we have used genome-wide DNA microarray studies to develop an expression signature associated with this phenotype. Using this signature, we identify a program of activated mitochondrial biogenesis associated with the phenotype of anchorage-independent growth and importantly, we demonstrate that this phenotype predicts potential for metastasis in primary breast and lung tumors. Keywords: c-Myc or v-Src retroviral vector-infected immortalized mouse embryonic fibroblasts. Expression data of c-Myc and v-Src transformed MEFs was used to validate an expression signature generated from human cultured breast cancer cell lines with anchorage-independent growth ability.
2009-04-10 | E-GEOD-15161 | biostudies-arrayexpress
Project description:Cultured cancer cells exhibit substantial phenotypic heterogeneity when measured in a variety of ways such as sensitivity to drugs or the capacity to grow under various conditions. Among these, the ability to exhibit anchorage-independent cell growth (colony forming capacity in semisolid media), has been considered to be fundamental in cancer biology, because it has been connected with tumor cell aggressiveness in vivo such as tumorigenic and metastatic potentials, and also utilized as a marker for in vitro transformation. Although multiple genetic factors for anchorage-independence have been identified, the molecular basis for this capacity is still largely unknown. To investigate the molecular mechanisms underlying anchorage independent cell growth, we have used genome-wide DNA microarray studies to develop an expression signature associated with this phenotype. Using this signature, we identify a program of activated mitochondrial biogenesis associated with the phenotype of anchorage-independent growth and importantly, we demonstrate that this phenotype predicts potential for metastasis in primary breast and lung tumors. Keywords: Breast cancer cell lines with various colony-forming ability
2009-04-10 | GSE15026 | GEO
Project description:Cultured cancer cells exhibit substantial phenotypic heterogeneity when measured in a variety of ways such as sensitivity to drugs or the capacity to grow under various conditions. Among these, the ability to exhibit anchorage-independent cell growth (colony forming capacity in semisolid media), has been considered to be fundamental in cancer biology, because it has been connected with tumor cell aggressiveness in vivo such as tumorigenic and metastatic potentials, and also utilized as a marker for in vitro transformation. Although multiple genetic factors for anchorage-independence have been identified, the molecular basis for this capacity is still largely unknown. To investigate the molecular mechanisms underlying anchorage independent cell growth, we have used genome-wide DNA microarray studies to develop an expression signature associated with this phenotype. Using this signature, we identify a program of activated mitochondrial biogenesis associated with the phenotype of anchorage-independent growth and importantly, we demonstrate that this phenotype predicts potential for metastasis in primary breast and lung tumors. Keywords: Breast cancer cell lines with various colony-forming ability To develop an expression signature reflecting the capacity for anchorage-independent cell growth, we first carried out colony formation assays with 19 breast cancer cell lines in suspension culture dish with methyl-cellulose containing media. Starting with 20,000 plated cells, five cell lines (MDA-MB-361, HCC38, ZR75, Hs578T and BT483) gave rise to less than 20 colonies, while 8 cell lines (MCF7, MDA-MB-231, BT20, SKBR3, MDA-MB-435s, T47D and BT474) showed formation of more than 500 colonies. The rest of the cell lines showed an intermediate phenotype in colony forming ability (20-200 colonies; HCC1143, HCC1806, HCC1428, MDA-MB-453, CAMA1, BT549 and MDA-MB-157). Among 19 cell lines, 11 cell lines have duplicates of expression data in a different batch. We removed the batch effect of this Affymetrix expression data using ComBat according to the instruction of http://statistics.byu.edu/johnson/ComBat/Abstract.html. Therefore, this dataset is a combined and standardized data that are originally RMA formatted.
2009-04-10 | E-GEOD-15026 | biostudies-arrayexpress
Project description:Cultured cancer cells exhibit substantial phenotypic heterogeneity when measured in a variety of ways such as sensitivity to drugs or the capacity to grow under various conditions. Among these, the ability to exhibit anchorage-independent cell growth (colony forming capacity in semisolid media) has been considered to be fundamental in cancer biology because it has been connected with tumor cell aggressiveness in vivo such as tumorigenic and metastatic potentials, and also utilized as a marker for in vitro transformation. Although multiple genetic factors for anchorage-independence have been identified, the molecular basis for this capacity is still largely unknown. To investigate the molecular mechanisms underlying anchorage-independent cell growth, we have used genome-wide DNA microarray studies to develop an expression signature associated with this phenotype. Using this signature, we identify a program of activated mitochondrial biogenesis associated with the phenotype of anchorage-independent growth and importantly, we demonstrate that this phenotype predicts potential for metastasis in primary breast and lung tumors. Keywords: c-Myc or v-Src retroviral vector-infected immortalized mouse embryonic fibroblasts.
2009-04-10 | GSE15161 | GEO
Project description:The ability of high-risk neuroblastoma to survive unfavorable growth conditions and multimodal therapy is hypothesized to result from a phenomenon known as reversible adaptive plasticity (RAP). RAP is a novel phenomenon enabling neuroblastoma cells to transition between a proliferative anchorage dependent (AD) state and a slow growing anoikis-resistant anchorage independent (AI) state. We used microarrays to investigate the global gene expression profiles in AD and AI cells, and to identify the differential expressed genes within signaling pathways contributing to the reversible adaptive plasticity between AD and AI cells.
2014-03-13 | GSE45160 | GEO
Project description:Reversible and irreversible anchorage independent growth in skin cells
| PRJNA110237 | ENA
Project description:Acquisition of independence from anchorage to the extracellular matrix is a critical event for onset and progression of solid cancers. To identify and characterize new genes conferring anchorage independence, we transduced MCF10A human normal breast cells with a retroviral cDNA expression library and selected them by growth in suspension. Microarray analysis targeted on library-derived transcripts revealed robust and reproducible enrichment, after selection, of cDNAs encoding the scaffolding adaptor Gab2. Gab2 was confirmed to strongly promote anchorage-independent growth when overexpressed. Interestingly, downregulation by RNAi of endogenous Gab2 in neoplastic cells did not affect their adherent growth, but abrogated their growth in soft agar. Gab2-driven anchorage independence was found to specifically involve activation of the Src-Stat3 signaling axis. A transcriptional “signature” of 205 genes was obtained from GAB2-transduced, anchorage-independent MCF10A cells, and found to contain two main functional modules, respectively controlling proliferation and cell adhesion/migration/invasion. Extensive validation on breast cancer datasets showed that the Gab2-signature provides a robust prognostic classifier for breast cancer metastatic relapse, largely independent from existing clinical and genomic indicators and from estrogen receptor status. This work highlights a pivotal role for GAB2 and its transcriptional targets in anchorage-independent growth and breast cancer metastatic progression.
2009-10-21 | GSE18237 | GEO
Project description:Triple-negative breast cancer (TNBC) is an aggressive subtype with few treatment options for chemo-resistant disease. In both preclinical models and patient circulating tumor cells, androgen receptor (AR) expression is increased in anchorage independent TNBC. The AR inhibitor enzalutamide (Enza) leads to reduced TNBC growth in soft agar, invasion, mammosphere formation in vitro, and reduced tumorigenicity and recurrence when combined with chemotherapy in vivo pre-clinical models. Transforming growth factor β (TGFβ) pathway gene signatures are also increased during TNBC anchorage independent survival both in vitro and in vivo in pre-clinical models and CTC from patients during relapse while on chemotherapy. We hypothesized that a positive loop between AR and TGFβ signaling facilitates TNBC anchorage independent survival (anoikis resistance). We previously published that AR protein levels and transcriptional activity increased during anchorage independent conditions and we now find that that multiple components of the TGFβ pathway, including TGFβ1 and 3, as well as pathway activity, as measured by nuclear localization and transcriptional activity of pSmad3, are enhanced in anchorage independent conditions. Indeed, exogenous TGFβ increased AR protein and TGFβ inhibition decreased AR and TNBC viability, particularly under anchorage independent culture conditions. ChIP-Seq experiments revealed AR binding to genomic regions near the TGFB1 and SMAD3. TGFB3 and AR expression were positively correlated in clinical datasets and high levels of co-expression correspond to significantly worse recurrence-free and overall survival in both ER- and basal-like breast cancer. Finally, combining Enza with a TGFβ inhibitor decreased cell survival more than either drug alone, particularly under anchorage independent conditions, where the effect was more than additive. These findings warrant further investigations into whether combined inhibition of AR and TGFβ pathways might decrease metastatic recurrence rates and mortality from TNBC.
2021-11-10 | GSE157862 | GEO
Project description:Cervical cancer and a subset of anogenital and head-and-neck carcinomas are caused by persistent infection with high-risk types of the human papillomavirus (hrHPV). Early stages of hrHPV-induced carcinogenesis can be faithfully mimicked in vitro. A major hallmark of hrHPV-transformed cells is their ability to grow anchorage independently, an oncogenic trait known to depend on inactivation of tumour suppressor genes. This study used an in vitro model of hrHPV-induced transformation to delineate in a longitudinal manner to what extent DNA methylation-mediated silencing of tumour suppressive microRNAs (miRNAs) contributed to hrHPV-induced anchorage independence. Genome-wide miRNA expression profiles were yielded from anchorage dependent (n=11) and independent passages (n=19) of 4 hrHPV-immortalised keratinocyte cell lines with and without demethylating treatment (DAC). Unsupervised clustering analysis showed that overall miRNA expression patterns discriminated between anchorage dependent and independent cells. Ten miRNA genes potentially silenced by methylation were selected and validated by bisulfite sequencing and methylation-specific PCR. Hsa-mir-129-2, -137, -935, -3663, -3665, and -4281 showed increased methylation in both HPV-transformed keratinocytes and cervical cancer cell lines compared to primary keratinocytes. Mature miRNAs derived from hsa-mir-129-2, -137, -3663, and -3665 decreased anchorage independence in cervical cancer cell lines. Finally, significantly increased methylation of hsa-mir-129-2, -935, -3663, -3665, and -4281 was observed in cervical (pre)cancerous lesions, underlining the clinical relevance of our findings. In conclusion, methylation-mediated silencing of tumour suppressive miRNAs contributes to the acquisition of anchorage independence, supporting the importance of miRNAs during early stages of carcinogenesis and underlining their potential as both disease markers and therapeutic targets.
2017-02-09 | GSE78278 | GEO
Project description:The ability of high-risk neuroblastoma to survive unfavorable growth conditions and multimodal therapy is hypothesized to result from a phenomenon known as reversible adaptive plasticity (RAP). RAP is a novel phenomenon enabling neuroblastoma cells to transition between a proliferative anchorage dependent (AD) state and a slow growing anoikis-resistant anchorage independent (AI) state. We used microarrays to investigate the global gene expression profiles in AD and AI cells, and to identify the differential expressed genes within signaling pathways contributing to the reversible adaptive plasticity between AD and AI cells. Comparison of microarray data from AD cells (n=4 independent cultures) versus AI cells (n=4 independent cultures) were performed using Partek Genomics Suite 6.5. Differentially expressed genes with an FDR M-bM-^IM-$5% and a fold-change M-bM-^IM-%1.5 were selected for pathway analysis.
2014-03-13 | E-GEOD-45160 | biostudies-arrayexpress