This SuperSeries is composed of the SubSeries listed below.
Early membrane initiated transcriptional effects of estrogens in breast cancer cells: First pharmacological evidence for a novel membrane estrogen receptor element (ERx).
Specimen part, Cell line
View SamplesIn humans with UC, low-grade dysplasia also develops predominantly in the distal colon, progresses more rapidly to neoplasia than proximal colon low-grade dysplasia and associates with worse patient prognosis. In a mouse model of colitis-associated carcinogenesis induced by administration of the mutagen AOM and the luminal toxin DSS, tumors also develop exclusively in the distal part of the large intestine. We monitored global changes in the transcriptome of mouse proximal and distal colon during exposure to AOM/DSS with the aim to define biological pathways and processes that characterize regional responses of the large intestine to colitis-associated carcinogenesis.
No associated publication
Sex, Specimen part
View SamplesEstrogens have been reported to activate several processes via membrane binding to either classic estrogen receptors (ERs) or GPR30. We have used either estradiol or BSA-conjugated estradiol in order to initiate membrane-initiated actions and ICI 172,780 (ICI) or G15 to explore ER- and GPR30-related transcription. Our results show that the majority of G15-inhibited transcription is depending on ERs, as it is also inhibited by ICI. However, a small number of transcripts, related to specific actions/pathways is either exclusively inhibited by G15, providing evidence about a specific GPR30 signature, or not inhibited by ICI or G15 suggesting the existence of another, yet unidentified estrogen receptor.
Early membrane initiated transcriptional effects of estrogens in breast cancer cells: First pharmacological evidence for a novel membrane estrogen receptor element (ERx).
Specimen part, Cell line
View SamplesEstrogens have been reported to activate several processes via membrane binding to either classic estrogen receptors (ERs) or GPR30. We have used either estradiol or BSA-conjugated estradiol in order to initiate membrane-initiated actions and ICI 172,780 (ICI) or G15 to explore ER- and GPR30-related transcription. Our results show that the majority of G15-inhibited transcription is depending on ERs, as it is also inhibited by ICI. However, a small number of transcripts, related to specific actions/pathways is either exclusively inhibited by G15, providing evidence about a specific GPR30 signature, or not inhibited by ICI or G15 suggesting the existence of another, yet unidentified estrogen receptor.
Early membrane initiated transcriptional effects of estrogens in breast cancer cells: First pharmacological evidence for a novel membrane estrogen receptor element (ERx).
Specimen part, Cell line
View SamplesAssessment of different subcellular localizations (membrane, cytosol, nucleus) of estrogen receptors by multi-epitope protein expression in 200 NSCLC specimens and matched non-cancerous tissues and ESR-1 probe mapping meta-analysis of Affymetrix 2.0 plus data in 1398 NSCLC tumors and normal lung tissues and 39 NSCLC cell lines led us to the conclusion that ER extranuclear variants are the main ERs in NSCLC. In order to further analyze these effects we treated A549 and H520 cell lines with 17-estradiol, 17-estradiol-BSA (plasma membrane impermeable conjugate) and tamoxifen for 3h, in order to investigate early transcriptional effects and responsiveness to estrogen agonists and antagonists.
No associated publication
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Whole transcriptome analysis of the ERα synthetic fragment P295-T311 (ERα17p) identifies specific ERα-isoform (ERα, ERα36)-dependent and -independent actions in breast cancer cells.
Cell line
View SamplesEstrogens have been reported to activate several processes via membrane binding to either classic estrogen receptors (ERs) or GPR30. We have used either estradiol or BSA-conjugated estradiol in order to initiate membrane-initiated actions and ICI 172,780 (ICI) or G15 to explore ER- and GPR30-related transcription. Our results show that the majority of G15-inhibited transcription is depending on ERs, as it is also inhibited by ICI. However, a small number of transcripts, related to specific actions/pathways is either exclusively inhibited by G15, providing evidence about a specific GPR30 signature, or not inhibited by ICI or G15 suggesting the existence of another, yet unidentified estrogen receptor.
Early membrane initiated transcriptional effects of estrogens in breast cancer cells: First pharmacological evidence for a novel membrane estrogen receptor element (ERx).
Specimen part, Cell line
View SamplesEstrogens have been reported to activate several processes via membrane binding to either classic estrogen receptors (ERs) or GPR30. We have used either estradiol or BSA-conjugated estradiol in order to initiate membrane-initiated actions and ICI 172,780 (ICI) or G15 to explore ER- and GPR30-related transcription. Our results show that the majority of G15-inhibited transcription is depending on ERs, as it is also inhibited by ICI. However, a small number of transcripts, related to specific actions/pathways is either exclusively inhibited by G15, providing evidence about a specific GPR30 signature, or not inhibited by ICI or G15 suggesting the existence of another, yet unidentified estrogen receptor.
Early membrane initiated transcriptional effects of estrogens in breast cancer cells: First pharmacological evidence for a novel membrane estrogen receptor element (ERx).
Specimen part, Cell line
View SamplesQuercetin is a flavonol modifying numerous cell processes with potent antiproliferative effects on cancer cell-lines. The aim of this study was to explore by gene-array analysis the effect of quercetin on cancer-related gene expression in HepG2 cells, followed by verification with RT-PCR and analysis of the expected phenotypic changes (migration, cell cycle, cell proliferation). Quercetin induces significant changes on cell-adhesion related genes, leading to reduced migratory capacity and disorganization of the actin cytoskeleton. Several genes related to DNA functions, cellular metabolism and signal-transducer activities were also modified, while an early effect on Gprotein related cascades possibly via protease-activated receptor 2 and phospholipase C-1 was identified. Cyclin-D associated events in G1 and ubiquitin-dependent degradation of cyclin-D1 were also affected, resulting in cell-cycle arrest without activation of apoptosis pathways. In conclusion quercetin (3M) exerts its cellular effects by modifying numerous genes related to mechanisms involved in cancer initiation and promotion.
Quercetin accumulates in nuclear structures and triggers specific gene expression in epithelial cells.
Cell line
View SamplesAnalysis of gene expression in proximal versus distal part of the mouse large intestine.
No associated publication
Sex, Specimen part
View Samples