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MiR-27b synergizes with anticancer drugs

ABSTRACT: Drug resistance, caused by complex and redundant mechanisms, is a major obstacle in cancer treatment, especially in liver and kidney cancers. Combinational therapy of miRNAs, which concurrently target multiple pathways, with anticancer drugs represent a new strategy to improve the drug response. By a systems approach, we identified that miR-27b, a miRNA deleted in liver and kidney cancers, sensitizes cancer cells to a broad spectrum of anticancer drugs in vitro and in vivo.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53872 | GEO | 2014/01/07

SECONDARY ACCESSION(S): PRJNA233607

REPOSITORIES: GEO

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miR-27b synergizes with anticancer drugs

Project description:Drug resistance, caused by complex and redundant mechanisms, is a major obstacle in cancer treatment, especially in liver and kidney cancers. Combinational therapy of miRNAs, which concurrently target multiple pathways, with anticancer drugs represent a new strategy to improve the drug response. By a systems approach, we identified that miR-27b, a miRNA deleted in liver and kidney cancers, sensitizes cancer cells to a broad spectrum of anticancer drugs in vitro and in vivo. Two samples transfected with nontarget miRNA control or miR-27b mimics followed by 48 hours doxorubicin treatment

2014-01-07 | E-GEOD-53872 | biostudies-arrayexpress

Homo sapiens

Project description:miR-27b synergizes with anticancer drugs

| PRJNA233607 | ENA

Mirabegron displays anticancer effects by globally browning adipose tissues

Project description:<p>Metabolic reprogramming in malignant cells is a hallmark of cancer that relies on augmented glycolytic metabolism to support their growth, invasion and metastasis. However, the impact of global adipose metabolism on tumor growth and the drug development by targeting adipose metabolism remain largely unexplored. Here we show that a therapeutic paradigm of drugs is effective for treating various cancer types by browning adipose tissues. Mirabegron, a clinically available drug for overactive bladders, displays potent anticancer effects in various animal cancer models, including untreatable cancers such as pancreatic ductal adenocarcinoma and hepatocellular carcinoma, via the browning of adipose tissues. Genetic deletion of the uncoupling protein 1 (UCP1), a key thermogenic protein in adipose tissues, ablates the anticancer effect. Similarly, the removal of brown adipose tissue (BAT), which is responsible for non-shivering thermogenesis, attenuates the anticancer activity of mirabegron. These findings demonstrate that mirabegron represents a paradigm of anticancer drugs with a distinct mechanism for the effective treatment of multiple cancers.</p>

2023-11-08 | MTBLS8682 | MetaboLights

Anticancer properties of distinct antimalaria drug classes

Project description:Background: Antimalarials have anticancer potential. Results: We have systematically tested five distinct antimalaria drugs in a panel of cancer cell lines. Conclusion: Three antimalarial classes display potent antiproliferative activity, and their potency is correlated with cancer cell gene expression patterns. Significance: We confirm and extend anticancer potential of these antimalarials and we discuss their therapeutic potential based on clinical data. Key words: Malaria, Anticancer drug, Drug Discovery, Genomics, Gene Expression, Bioinformatics, Cancer AffymetrixM-BM-. HG-U133 Plus 2.0 mRNA expression arrays were used to determine the expression. CEL result files were pre-processed using the RMA (Irizarry et al, 2003) algorithm. This microarray analysis was performed for 91 cell lines.

2013-10-26 | E-GEOD-51739 | biostudies-arrayexpress

Anticancer properties of distinct antimalaria drug classes

2013-10-26 | GSE51739 | GEO

Epigenetic regulation of the DNMT1/MT1G/KLF4/CA9 axis synergizes the anticancer effects of sorafenib in hepatocellular carcinoma

Project description:Sorafenib, a multiple-kinase inhibitor, has been widely used as a first-line anticancer drug for advanced hepatocellular carcinoma (HCC). However, the development of drug resistance to sorafenib is frequently observed in clinical applications. Potential non-kinase targets of sorafenib have not been well documented and may provide insights into reversing drug resistance. Herein, we report that sorafenib exerted its anticancer effects by activating metallothionein 1G (MT1G) expression. MT1G served as a novel marker in HCC and correlated well with patient survival. MT1G overexpression suppressed the cellular proliferation, migration, invasion, and tumor formation of HCC, and sensitized cells to sorafenib treatment. However, the disruption of MT1G attenuated sorafenib’s anticancer effects. Mechanistically, sorafenib upregulated MT1G expression via hypomethylation of its promoter region by binding and inhibiting DNA methyltransferase 1 (DNMT1) and increasing its promoter accessibility in HCC cells. The activation of MT1G also inhibited CA9 transcription through the degradation of HIF1a as mediated by KLF4. Our collective data revealed that sorafenib exerted its anticancer effects through epigenetic regulation of the DNMT1/MT1G/KLF4/CA9 axis in HCC, and that the activation of MT1G might constitute a strategy for reversing sorafenib resistance.

2022-04-30 | GSE192771 | GEO

miR-27b synergizes with anticancer drugs via p53 activation and CYP1B1 suppression.

Project description: Not available

| S-EPMC4387554 | biostudies-literature

Identification of microRNA-27b target genes in breast cancer cell lines

2015-06-18 | GSE67631 | GEO

Identification of microRNA-27b target genes in breast cancer cell lines

Project description:To identify the microRNA-27b (miR-27b) target genes in luminal-type breast cancer cells, we performed the microarray analysis using miR-27b knockdown MCF7-luc cell line (MCF7-luc anti-miR-27b), miR-27b overexpressing MCF7-luc cell line (MCF7-luc miR-27b o.e.) and their contro cell line (MCF7-luc anti-NC). After establishing MCF7-luc anti-miR-27b, MCF7-luc miR-27b o.e. and MCF7-luc anti-NC using lentivirus vector, we performed the microarray analysis.

2015-06-18 | E-GEOD-67631 | biostudies-arrayexpress

Drug-induced change in gene expression across NCI-60 cell lines after exposure to 15 anticancer agents for 2, 6 and 24h

Project description:To identify patterns of drug-induced gene modulation that occur across different cell types, we measured gene expression changes across NCI-60 cell lines after exposure to 15 anticancer agents. The results were integrated into a database and set of interactive analysis tools, the NCI Transcriptional Pharmacodynamics Workbench (NCI TPW), intended to allow exploration of gene expression modulation, including by molecular pathway, drug target, and association with drug sensitivity. We identified common transcriptional responses across drugs and cell types and uncovered cell signaling pathway–specific gene expression changes associated with drug sensitivity. We also demonstrated the value of this tool for investigating clinically relevant molecular hypotheses, utilizing the NCI TPW to assess drug-induced expression changes in genes associated with immune function and epithelial-mesenchymal transition, and to identify candidate biomarkers for drug activity. The NCI TPW provides a comprehensive resource to facilitate understanding of tumor cell characteristics that define sensitivity to anticancer drugs.

2018-10-09 | GSE116436 | GEO

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