Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE15181
PROVIDER: PRJNA123207 | 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: 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: 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: 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:TWIST2 is deregulated in about 1/3 human acute myeloid leukemia (AML) patients partially due to hypermethylation. Overexpression of TWIST2 in various AML cell lines and primary AML cells leads to growth arrest, reduced colony forming cell (CFC) capacity, inhibited cell migration and tumorigenic ability in nude mice, suggesting its tumor suppressor role in AML. To explore the molecular insight of how TWIST2 acts as a tumor suppressor in AML cells, control and TWIST2 expressed THP-1 cells have been analyzed with microarray.
2014-05-07 | GSE57347 | GEO
Project description:Epigenetic portraits of human breast cancers (various cell lines expression data)
| PRJNA128647 | ENA
Project description:Epigenetic portraits of human breast cancers (various cell lines methylation data)
| PRJNA128711 | ENA
Project description:TWIST2 is deregulated in about 1/3 human acute myeloid leukemia (AML)M-BM- patients partially due to hypermethylation. Overexpression of TWIST2 in various AML cell lines and primary AML cells leads to growth arrest, reduced colony forming cell (CFC) capacity, inhibited cell migration and tumorigenic ability in nude mice, suggesting its tumor suppressor role in AML. To explore the molecular insight of how TWIST2 acts as a tumor suppressor in AML cells, control and TWIST2 expressed THP-1 cells have been analyzed with microarray. 4 independent biological replicates of control and TWIST2 expressed THP-1 cells have been used for RNA extraction and microarray analysis with Agilent platform.
2014-05-07 | E-GEOD-57347 | biostudies-arrayexpress