Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1103179 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28769256_1.fastq.gz | Fastqsanger.gz | |||
| SRR28769256_2.fastq.gz | Fastqsanger.gz | |||
| SRR28769257_1.fastq.gz | Fastqsanger.gz | |||
| SRR28769257_2.fastq.gz | Fastqsanger.gz | |||
| SRR28769258_1.fastq.gz | Fastqsanger.gz |
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Project description:Propofol is an intravenous anesthetic that has been widely used in the clinical setting. Besides its anesthetic effects, propofol has been reported to influence the regulation of autonomic system. Controversies exist with regards to whether propofol exposure is safe for pregnant women and young children. The recent emergence of human induced pluripotent stem cells (hiPSCs) has provided a promising and theoretically inexhaustible source of neural progenitor cells (NPCs) for drug testing, which could be extended to in vitro experiments for anesthetics such as propofol. NPCs derived from three hiPSC lines, NES-GFP (a NESTIN-GFP reporter), USCK7 (iPSCs derived from urine derived cells), and ND2-0 (NIH), were treated with propofol at different concentrations (20, 50, 100 and 300 µM) for 6 h or 24 h. Early and late cell injury, cell proliferation and apoptosis were evaluated. Comparison of genome-wide gene expression profiles was performed for propofol-treated and untreated control iPSC-NPCs. Propofol treatment of NPCs for 6 h at the clinically relevant concentration (20 or 50 µM) did not affect cell viability, apoptosis, or proliferation, while propofol at higher concentration (100 or 300 µM) decreased NPC viability and induced apoptosis. Prolonged treatment of propofol for 24 h significantly decreased cell viability. In addition, 20 µM propofol treatment for 6 h did not alter global gene expression. Higher concentration of propofol exerted potential cytotoxicity via multiple cellular mechanisms. In summary, propofol treatment at commonly practiced clinical doses for 6 h did not have adverse effects on hiPSC-derived NPCs. In contrast, longer exposure and/or higher concentration of propofol treatment could decrease NPC viability and induce apoptosis.
2017-07-21 | GSE101724 | GEO
Project description:Anesthetic management of heart failure patients undergoing noncardiac surgery remains challenging due to cardiac suppressive properties of anesthetics. Due to varying electrophysiological properties, small and large animals are not good models for studying human myocardial anesthetic responses. Here we use hypertrophic (HCM), dilated (DCM) and healthy human induced pluripotent stem cells derived cardiomyocytes (hiPSC-CMs) to evaluate the cardiac suppression of propofol and etomidate. We demonstrate that propofol and etomidate act through GABAA receptors and contractile inhibition can occur without cell-cell junction. At supraphysiological dosage (100mM), we discovered that cardiac suppression induced by etomidate is reversible while propofol is not. Using transcriptome profiling, we uncover that etomidate was capable of inducing autophagy, likely through induction of cytosolic calcium. Lack of autophagy induction in propofol treated cardiomyocytes were associated with increased apoptosis. Together, we provide the robustness of using hiPSC-CMs as an in vitro cardiotoxicity platform for anesthetics. To delineate how etomidate confers cardioprotection during contraction inhibition, we performed transcriptome profiling on DCM hiPSC-CMs treated with either 10 μM propofol, 10 μM etomidate or DMSO control.
2022-08-30 | GSE212044 | GEO
Project description:Efficacy and safety of anticancer drugs are traditionally studied using cancer cell lines and animal models. Recently, a potential anticancer agent, JQ1, an inhibitor of bromodomain and extra terminal (BET) protein, has been shown to promote apoptosis of cancerous cells by arresting them in G1 phase of the cell cycle. However, the effect of JQ1 on normal cells is poorly understood. In this study, we investigated the safety of JQ1 by using human umbilical cord mesenchymal stem cells (MSCs) as an in vitro model system. Our results indicated that JQ1 induced cell cycle arrest in G1 phase of MSCs, but did not promote apoptosis. Microarray analysis of MSCs treated with JQ1 indicated that it down-regulated genes involved not only in cell cycle regulation but also DNA replication, mitosis, and cell division. Although many studies have suggested the potential of JQ1 as an anticancer agent, our findings suggest that it caused a deleterious effect on normal cells and may not be safe for anticancer therapy. Human umbilical cord derived MSCs were cultured in vitro and treated with either 100 nM or 500 nM JQ1 for 24 hrs. Gene expression of treated cells was compared to untreated cultured cells.
2016-02-12 | E-GEOD-70577 | biostudies-arrayexpress
Project description:Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor α1 apoprotein. Basal proliferation persisted in estrogen-sensitive breast cancer cells grown in hormone depleted conditioned media without or with 4-hydroxytamoxifen (OH-Tam). Downregulating ER using siRNA inhibited basal proliferation by promoting cell cycle arrest. The basal expression of RARα1, the only RARα isoform that was expressed in breast cancer cell lines and in most breast tumors, was supported by apo-ER but was unaffected by OH-Tam. The overlapping tamoxifen-insensitive gene regulation by apo-ER and apo-RARα1 comprised activation of mainly genes promoting cell cycle and mitosis and suppression of genes involved in growth inhibition.
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Project description:Triple-negative breast cancer (TNBC) is difficult to treat due to the lack of biological targets and poor sensitivity to conventional therapies. Chemotherapy is the main treatment in the clinic, but there is still no effective screening strategy for chemotherapy drugs. Several studies have attempted to find the pathogenesis through sequencing, but the integration of transcriptome maps of various tumors for drug discovery has been slow. Drug repurposing has attracted increasing attention in recent years. We first found there were common features between leukemia and TNBC. Therefore, we chose a classic leukemia drug thioguanine (6-TG) as a candidate drug. We utilized RNA-seq and DNA methylation arrays to evaluate its role in MDA-MB-231 cells. Our results demonstrated that 6-TG inhibited cell proliferation by suppressing PI3K-AKT pathway via downregulating the DNA methylation level of PTEN. Moreover, apoptosis was induced via the activation of PI3K-AKT downstream molecular TSC1 and the downregulation of methylation levels of DAXX, TNF, FADD and CASP8 etc., these genes involved in apoptosis pathways. 6-TG presents anti-tumor effects in vitro and vivo by regulating the DNA methylation levels of PI3K-AKT pathway and apoptosis pathway. Meanwhile, we proved transcriptome-based drug screening has potential implications for breast cancer therapy and drug selection.
2022-01-01 | GSE137418 | GEO
Project description:Efficacy and safety of anticancer drugs are traditionally studied using cancer cell lines and animal models. Recently, a potential anticancer agent, JQ1, an inhibitor of bromodomain and extra terminal (BET) protein, has been shown to promote apoptosis of cancerous cells by arresting them in G1 phase of the cell cycle. However, the effect of JQ1 on normal cells is poorly understood. In this study, we investigated the safety of JQ1 by using human umbilical cord mesenchymal stem cells (MSCs) as an in vitro model system. Our results indicated that JQ1 induced cell cycle arrest in G1 phase of MSCs, but did not promote apoptosis. Microarray analysis of MSCs treated with JQ1 indicated that it down-regulated genes involved not only in cell cycle regulation but also DNA replication, mitosis, and cell division. Although many studies have suggested the potential of JQ1 as an anticancer agent, our findings suggest that it caused a deleterious effect on normal cells and may not be safe for anticancer therapy.
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Project description:Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor M-NM-11 apoprotein. Basal proliferation persisted in estrogen-sensitive breast cancer cells grown in hormone depleted conditioned media without or with 4-hydroxytamoxifen (OH-Tam). Downregulating ER using siRNA inhibited basal proliferation by promoting cell cycle arrest. The basal expression of RARM-NM-11, the only RARM-NM-1 isoform that was expressed in breast cancer cell lines and in most breast tumors, was supported by apo-ER but was unaffected by OH-Tam. The overlapping tamoxifen-insensitive gene regulation by apo-ER and apo-RARM-NM-11 comprised activation of mainly genes promoting cell cycle and mitosis and suppression of genes involved in growth inhibition. Cells were plated at 20% confluence in low glucose phenol red free medium supplemented with 5% charcoal stripped FBS and glutamine 24h-48h prior to transfection. Treatment with vehicle, OH-Tam (100nM), or OH-Tam (500nM) was begun an additional 24h later. Cells were transfected with control siRNA, ERM-NM-1 siRNA or RARM-NM-1 siRNA.
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Project description:We recently discovered an unexpected reversibility of execution-stage apoptosis in vitro and in vivo, and coined the term anastasis (Greek for “rising to life”) for this cell recovery phenomenon. Promoting anastasis could in principle preserve injured cells that are difficult to replace such as cardiomyocytes and neurons. Conversely, arresting anastasis in dying cancer cells after cancer therapies could improve treatment efficacy. To harness the discovery of anastasis to develop revolutionary new therapies, it is essential to identify the key regulators of anastasis – the therapeutic targets. Therefore, we performed microarray analysis to study the molecular mechanism of anastasis using reversal of ethanol-induced apoptosis in mouse primary liver cells as a model. Our data reveal active transcription involved in multiple pathways during anastasis, including early activation of pro-survival genes, cell cycle arrest, anti-p53-mediated DNA damage response, and at delayed times, stress-inducible responses such as cell migration. Here, we present a dataset containing the time-course gene expression profiles during apoptosis reversal, which has implications for the physiological, pathological, and therapeutic implications of anastasis.
2022-05-23 | GSE90959 | GEO
Project description:The molecular mechanisms underlying estrogen receptor (ER)-positive breast carcinogenesis and endocrine therapy resistance remain incompletely understood. Here, we reported that circPVT1, a circular RNA generated from lncRNA PVT1, is highly expressed in ERalpha-positive breast cancer cell lines and tumor samples, which is functionally important in promoting ERalpha-positive breast tumorigenesis and endocrine therapy resistance. CircPVT1 acts as a competing endogenous RNA (ceRNA) to sponge miR-181a-2-3p, promoting the expression of ESR1 and downstream ERalpha-target genes and breast cancer cell growth. Meanwhile, circPVT1 directly interacts with MAVS to disrupt the RIGI-MAVS complex formation, inhibiting type I interferon (IFN) signaling pathway and anti-tumor immunity. The dual mechanisms both contribute to ERα-positive breast tumorigenesis. Anti-sense oligonucleotides (ASO) targeting circPVT1 was shown to inhibit ERalpha-positive breast cancer cell and tumor growth, and could re-sensitize tamoxifen-resistant ERalpha-positive breast cancer cells to tamoxifen treatment. Taken together, our data demonstrated that circPVT1 can work through both ceRNA and protein scaffold mechanisms to promote cancer, and in particular, circPVT1 may serve as a diagnosis biomarker and therapeutic target for ERalpha-positive breast cancer in the clinic.
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