Single-cell comparative transcriptomics of control and MK-886-treated sea urchin primary mesenchyme cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Lytechinus variegatus
PROVIDER: GSE164240 | GEO | 2022/06/01
REPOSITORIES: GEO
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Project description:MK: MK-801. Young male C57BL/6J mice received an injection of MK-801 (300 micro-g per g body weight). RNA from control mice were extracted 1hr, 2hr, 4hr, and 6hr after MK experimental mice received their last shock treatment. MK C+S: MK-801 & Context + Shock: Young male C57BL/6J mice received an injection of MK-801 (300 micro-g per g body weight) 1 h prior to contextual fear conditioning that consisted of: Placement into a novel spatial context for 2 min. After 2 min, a 1 sec (0.5 mA) shock was administered through a floor grid. The 2 min-1 sec shock paradigm was repeated for a total of 3 shocks. 1 min after the last shock, animals were removed to their homecage. RNA was extracted 1hr, 2hr, 4hr, and 6hr after the last shock treatment. Keywords: time-course
2003-02-27 | GSE318 | GEO
Project description:MK: MK-801. Young male C57BL/6J mice received an injection of MK-801 (300 micro-g per g body weight). RNA from control mice were extracted 1hr, 2hr, 4hr, and 6hr after MK experimental mice received their last shock treatment. MK C+S: MK-801 & Context + Shock: Young male C57BL/6J mice received an injection of MK-801 (300 micro-g per g body weight) 1 h prior to contextual fear conditioning that consisted of: Placement into a novel spatial context for 2 min. After 2 min, a 1 sec (0.5 mA) shock was administered through a floor grid. The 2 min-1 sec shock paradigm was repeated for a total of 3 shocks. 1 min after the last shock, animals were removed to their homecage. RNA was extracted 1hr, 2hr, 4hr, and 6hr after the last shock treatment. Keywords: time-course
2003-02-27 | GSE317 | GEO
Project description:Introduction: Mammalian target of rapamycin (mTOR) represents a key downstream intermediate for a myriad of oncogenic receptor tyrosine kinases. In the case of the insulin-like growth factor (IGF) pathway, the mTOR complex (mTORC1) mediates IGF-1 receptor (IGF-1R)-induced estrogen receptor alpha (ERα) phosphorylation/activation and leads to increased proliferation and growth in breast cancer cells. As a result, the prevalence of mTOR inhibitors combined with hormonal therapy has increased in recent years. Conversely, activated mTORC1 provides negative feedback regulation of IGF signaling via insulin receptor substrate (IRS)-1/2 serine phosphorylation and subsequent proteasomal degradation. Thus, the IGF pathway may provide escape (e.g. de novo or acquired resistance) from mTORC1 inhibitors. It is therefore plausible that combined inhibition of mTORC1 and IGF-1R for select subsets of ER-positive breast cancer patients presents as a viable therapeutic option. Methods: Using hormone-sensitive breast cancer cells stably transfected with the aromatase gene (MCF-7/AC-1), works presented herein describe the in vitro and in vivo antitumor efficacy of the following compounds: dalotuzumab (DALO; âMK-0646â; anti-IGF-1R antibody), ridaforolimus (RIDA; âMK-8669â; mTORC1 small molecule inhibitor) and letrozole (âLETâ, aromatase inhibitor). Results: With the exception of MK-0646, all single agent and combination treatment arms effectively inhibited xenograft tumor growth, albeit to varying degrees. Correlative tissue analyses revealed MK-0646 alone and in combination with LET induced insulin receptor alpha A (InsR-A) isoform upregulation (both mRNA and protein expression), thereby further supporting a triple therapy approach. Conclusion: These data provide preclinical rationalization towards the combined triple therapy of LET plus MK-0646 plus MK-8669 as an efficacious anti-tumor strategy for ER-positive breast tumors. 46 samples, 28 days post treatment
2016-07-01 | E-GEOD-79492 | biostudies-arrayexpress
Project description:Local administration of IFN-α-producing proliferating myeloid cells (IFN-α-iPSC-pMCs) inhibited the tumor growth not only at the treatment site (right) but also at the distant site (left). We identified genes with log fold expression change ≥ 1 or ≤ −1 in untreated versus IFN-α-iPSC-pMC-treated tumors and iPSC-pMC-treated versus IFN-α-iPSC-pMC-treated tumors for treatment or distant site, respectively. Of the overlapping genes differentially expressed in IFN-α-iPSC-pMC-treated mice, 301/671 distant site and 460/928 treated site genes were ISGs, of which 95.3% and 94.7%, respectively, were type I IFN-related. By gene ontology, the up-regulated ISG signatures were enriched for “T cell-mediated immune responses”, “cytolysis”, and “migration of immune cells” associated genes. Collectively, Local administration of IFN-α-iPSC-pMCs alters the tumor microenvironment and propagates molecular signature associated with type I IFN.
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Project description:Introduction: Mammalian target of rapamycin (mTOR) represents a key downstream intermediate for a myriad of oncogenic receptor tyrosine kinases. In the case of the insulin-like growth factor (IGF) pathway, the mTOR complex (mTORC1) mediates IGF-1 receptor (IGF-1R)-induced estrogen receptor alpha (ERα) phosphorylation/activation and leads to increased proliferation and growth in breast cancer cells. As a result, the prevalence of mTOR inhibitors combined with hormonal therapy has increased in recent years. Conversely, activated mTORC1 provides negative feedback regulation of IGF signaling via insulin receptor substrate (IRS)-1/2 serine phosphorylation and subsequent proteasomal degradation. Thus, the IGF pathway may provide escape (e.g. de novo or acquired resistance) from mTORC1 inhibitors. It is therefore plausible that combined inhibition of mTORC1 and IGF-1R for select subsets of ER-positive breast cancer patients presents as a viable therapeutic option. Methods: Using hormone-sensitive breast cancer cells stably transfected with the aromatase gene (MCF-7/AC-1), works presented herein describe the in vitro and in vivo antitumor efficacy of the following compounds: dalotuzumab (DALO; “MK-0646”; anti-IGF-1R antibody), ridaforolimus (RIDA; “MK-8669”; mTORC1 small molecule inhibitor) and letrozole (“LET”, aromatase inhibitor). Results: With the exception of MK-0646, all single agent and combination treatment arms effectively inhibited xenograft tumor growth, albeit to varying degrees. Correlative tissue analyses revealed MK-0646 alone and in combination with LET induced insulin receptor alpha A (InsR-A) isoform upregulation (both mRNA and protein expression), thereby further supporting a triple therapy approach. Conclusion: These data provide preclinical rationalization towards the combined triple therapy of LET plus MK-0646 plus MK-8669 as an efficacious anti-tumor strategy for ER-positive breast tumors.
2016-07-01 | GSE79492 | GEO
Project description:Sal: Saline. Young male C57BL/6J mice received an injection of saline (5 microL per g body weight). RNA from control mice were extracted 1hr, 2hr, 4hr, and 6hr after MK experimental mice received their last shock treatment. MK: MK-801. Young male C57BL/6J mice received an injection of MK-801 (300 micro-g per g body weight). RNA from control mice were extracted 1hr, 2hr, 4hr, and 6hr after MK experimental mice received their last shock treatment. Keywords: time-course
2003-02-27 | GSE316 | GEO
Project description:Sal: Saline. Young male C57BL/6J mice received an injection of saline (5 microL per g body weight). RNA from control mice were extracted 1hr, 2hr, 4hr, and 6hr after MK experimental mice received their last shock treatment. MK: MK-801. Young male C57BL/6J mice received an injection of MK-801 (300 micro-g per g body weight). RNA from control mice were extracted 1hr, 2hr, 4hr, and 6hr after MK experimental mice received their last shock treatment. Keywords: time-course
2003-02-27 | GSE315 | GEO
Project description:We previously established a method to generate myeloid lineage cells with proliferation capacity from induced pluripotent stem cells (iPSCs) (Zhang R. Cancer Immunol Res. 3: 668, 2015). In this study, we generated the IFN-α-producing cells by genetic engineering of mouse iPSC-derived myeloid cells (iPSC-pMCs). Gene expression profiling of IFN-α-producing iPSC-pMCs (IFN-α-iPSC-pMCs) revealed a distinct interferon-stimulated gene (ISG) signature: of 613 differentially expressed genes (versus iPSC-pMC), 345 genes were ISGs of which > 70 % were type I IFN-related. Gene ontology analysis showed that the up-regulated gene signature was enriched for transcripts associate with immune responses, cellular responses to type I IFN, and defense responses to virus.
2019-02-13 | GSE126277 | GEO
Project description:Physical factors can have major influences on the proliferation and differentiation fate of hematopoietic stem cells in culture. Recently, we demonstrated that cord blood CD34+ cells undergo accelerated and increased megakaryocyte differentiation when incubated at 39°C. In this study, we investigated in detail the impacts of mild hyperthermia on the kinetics of megakaryocyte differentiation, maturation, polyploidization and cell viability. The qualitative and quantitative effects on Mk differentiation were found to be rapidly induced, and optimization of the culture length at 39°C led to greater Mk yields. Mild hyperthermia did not promote endomitosis of cord blood-derived Mk, but rather led to a small reduction in the proportion of polyploid Mk. Moreover, it had little impact on viability but induced a significant shift in the proportion of cells undergoing apoptosis at 37°C to necrosis at 39°C. Finally, our results suggest that the effects on megakaryocyte differentiation could be the consequences of aberrant expression of key megakaryocyte transcription factors induced by mild hyperthermia. Keywords: Effect of mild hyperthermia on Mk differentiation
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