The goal of this study was to compare the transcriptional responses of mouse macrophages treated with unsaturated or saturated fatty acids to macrophages treated with LPS to stimulate classical inflammatory activation.
Saturated Fatty Acids Engage an IRE1α-Dependent Pathway to Activate the NLRP3 Inflammasome in Myeloid Cells.
Specimen part, Treatment
View SamplesTo investigate the role of NKX3.1 in prostate differentiation, we employed transcriptome analysis of mouse seminal vesicle (from 15-month-old Nkx3.1+/+ mice); mouse prostate (from 4-month-old Nkx3.1+/+ and Nkx3.1-/- mice); human prostate cells (RWPE1 cells engineered with empty vector (altered pTRIPZ), NKX3.1 wild type over-expression, and NKX3.1 (T164A) mutant over-expression); and tissue recombinants (generated from combining engineered mouse epithelial cells (seminal vesicle epithelial cells or prostate epithelial cells from 2-month-old mice) and rat UGS mesenchymal cells). Mouse tissue or human cells were snap frozen for subsequent molecular analysis.
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Age, Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Predicting Drug Response in Human Prostate Cancer from Preclinical Analysis of In Vivo Mouse Models.
Specimen part, Disease, Disease stage, Treatment
View SamplesAnalysis of the transcriptome of mouse models of prostate cancer after treatment with rapamycin and PD0325901 combination therapy or standard of care docetaxel. The Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) was used in this study. Two months after tumor induction, mice were randomly assigned to vehicle (Veh) or treatments groups, such as rapamycin and PD0325901 (RAPPD) or docetaxel (Docetaxel). For the treatment groups mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) or docetaxel (10 mg/kg) for 5 days (SHORT) or for 1 month (LONG). At the end of the treatment, mice were euthanized, tumors harvested and snap frozen for subsequent molecular analysis.
Predicting Drug Response in Human Prostate Cancer from Preclinical Analysis of In Vivo Mouse Models.
Specimen part, Treatment
View SamplesAnalysis of transcriptome of tissue recombinants (mouse seminal vesicle epithelial [SVE] cells or prostate epithelial [PE] cells, and rat urogenital sinus [UGS] mesenchymal cells) grown under the kidney capsule in athymic nude mice for 3 months. Overall design: Total RNA obtained from tissue recombinants generated from combining engineered mouse epithelial cells (SVE or PE from 2-month-old C57Bl/6J mice) and rat UGS mesenchymal cells. Tissue recombinants were harvested and processed for RNA isolation and transcriptome analysis using the RNeasy kit (Qiagen).
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Age, Specimen part, Subject
View SamplesAnalysis of transcriptome of human RWPE1 cells over-expressing wild type NKX3.1 and mutant NKX3.1 (T164A). Overall design: Total RNA obtained from RWPE1 cells engineered with empty vector (altered pTRIPZ), NKX3.1 wild type over-expression, and NKX3.1 (T164A) mutant over-expression. Engineered RWPE1 cells were harvested and processed for RNA isolation and transcriptome analysis using the MagMAX RNA isolation kit (Ambion).
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Cell line, Subject
View SamplesAnalysis of transcriptome of prostate tissue from 4-month-old Nkx3.1 +/+ and Nkx3.1 -/- mice. Overall design: Total RNA obtained from prostate tissues from 4-month-old Nkx3.1 +/+ and Nkx3.1 -/- mice. Prostate tissues were harvested and processed for RNA isolation and transcriptome analysis using the MagMAX RNA isolation kit (Ambion).
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Age, Specimen part, Subject
View SamplesAnalysis of the transcriptome of allografted mouse tumors after treatment with rapamycin and PD0325901. Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) were induced and their tumors removed to generate allograft lines by implanting a 1.5 mm3 tumor fragment in the subcutaneous space of athymic nude mice. Allografted NPK tumors were allowed to grow until they reached a volume of 1 cm3, at which moment they were randomly assigned to either vehicle (Veh) or combination therapy using rapamycin and PD0325901 (RAPPD). Allografted mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) during five consecutive days (Allo SHORT). Mice were euthanized in the fifth day 6 hours after having received the last treatment and the tumors were harvested and snap frozen for subsequent molecular analysis.
Predicting Drug Response in Human Prostate Cancer from Preclinical Analysis of In Vivo Mouse Models.
Specimen part, Disease, Disease stage, Treatment
View SamplesAnalysis of transcriptome of seminal vesicle from 15-month-old Nkx3.1+/+ mice.
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Age, Specimen part
View SamplesTo identify MED1 target genes involved in prostate tumorigenesis.
ERK and AKT signaling drive MED1 overexpression in prostate cancer in association with elevated proliferation and tumorigenicity.
Specimen part, Cell line
View Samples