This 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 SamplesER17p is a synthetic peptide corresponding to the sequence P295LMIKRSKKNSLALSLT311 of the estrogen receptor alpha (ER) and initially synthesized to mimic its calmodulin binding site. ER17p was subsequently found to elicit estrogenic responses in E2-deprived ER-positive breast cancer cells, increasing proliferation and E2-dependent gene transcription. Surprisingly, in E2-supplemented media, ER17p induced apoptosis and modified the actin network, influencing thereby cell motility. Here, we report that ER17p induces a massive early (3h) transcriptional activity in breast cancer cell lines SKBR3). Remarkably, about 75% of the significantly modified transcripts were also modified by E2, confirming the pro-estrogenic profile of ER17p. The different ER spectra of the used cell lines allowed us to extract a specific ER17p signature related to ER and its variant ER36. With respect to ER, the peptide activates nuclear (cell cycle, cell proliferation, nucleic acid and protein synthesis) and extranuclear signaling pathways. In contrast, through ER36 it exerts inhibitory events on inflammation and cell cycle and inhibition of EGFR signaling. This is the first work reporting ER36 specific transcriptional effects. The fact that a number ER17p-induced transcripts is different from those activated by E2 revealed that the apoptosis and actin modifying effects of ER17p are independent from the ER-related actions of the peptide.
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 SamplesER17p is a synthetic peptide corresponding to the sequence P295LMIKRSKKNSLALSLT311 of the estrogen receptor alpha (ER) and initially synthesized to mimic its calmodulin binding site. ER17p was subsequently found to elicit estrogenic responses in E2-deprived ER-positive breast cancer cells, increasing proliferation and E2-dependent gene transcription. Surprisingly, in E2-supplemented media, ER17p induced apoptosis and modified the actin network, influencing thereby cell motility. Here, we report that ER17p induces a massive early (3h) transcriptional activity in breast cancer cell line MDA-MB-231.
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 SamplesER17p is a synthetic peptide corresponding to the sequence P295LMIKRSKKNSLALSLT311 of the estrogen receptor alpha (ER) and initially synthesized to mimic its calmodulin binding site. ER17p was subsequently found to elicit estrogenic responses in E2-deprived ER-positive breast cancer cells, increasing proliferation and E2-dependent gene transcription. Surprisingly, in E2-supplemented media, ER17p induced apoptosis and modified the actin network, influencing thereby cell motility. Here, we report that ER17p induces a massive early (3h) transcriptional activity in breast cancer cell line T47D.
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 SamplesThis 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 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 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 SamplesObjective: Transcriptional profiling of murine HSPC in response to ß-glucan-induced innate immune training Overall design: HSPC mRNA profiles of wild type (WT) mice injected with PBS or ß-glucan. Wild type (WT) C57BL/6 mice were intraperitoneally injected with PBS or 1 mg ß-glucan in PBS. Mice were sacrificed on day 7 or day 28 and long-term heematopoietic stem cells (LT-HSC) and/or multipotent progenitors (MPP) were sorted. In another group, mice were injected with PBS or 1 mg ß-glucan in PBS and on day 7 they were additionally injected with 150 mg/kg 5-fluouracil. Mice were sacrificed on day 14 after 5-FU administration and LT-HSC were sorted.
Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity.
Age, Specimen part, Cell line, Subject
View Samples