Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA280763 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer
| PRJNA280760 | ENA
Project description:Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer [miRNA]
| PRJNA280762 | ENA
Project description:Endotoxin/LPS tolerance is a tightly regulated phenomenon, which, during infection, prevents systemic hyper-inflammation. Here we report for the first time that morphine reversal of endotoxin tolerance resulting in persistent inflammation thus contributing to septicemia and septic shock. We further report that this regulation is mediated by LPS-induced down-regulation of microRNAs 146a and 155. However, only over-expression of miR-146a, but not miR-155 abrogates morphine mediated hyper-inflammation, while antagonizing miR-146a (but not miR-155) augments morphine mediated hyper-inflammation. Hence, miR-146a could be the potential therapeutic target for morphine-mediated abrogation of endotoxin tolerance. All treatments done in vivo. Morphine implanted subcuteniously, LPS administered as intraperitoneal injection.
2013-08-01 | E-GEOD-42506 | biostudies-arrayexpress
Project description:This experiment is designed to evaluate gene expression alteration and significant pathway(s) following miR-128 transduction in A549 lung cancer cells. We find several significant pathways, including the Wnt/β-catenin signaling and TGF-β signaling activated by miR-128 overexpression. Total RNA were extracted from A549 lung cancer cells stably transduced with miR-128 precursor or vector control and subjected to mRNA microarray (Agilent-014850 Whole Human Genome Microarray 4x44K) analysis, with two biological replications for each treatment.
2015-04-10 | E-GEOD-67728 | biostudies-arrayexpress
Project description:Endotoxin/LPS tolerance is a tightly regulated phenomenon, which, during infection, prevents systemic hyper-inflammation. Here we report for the first time that morphine reversal of endotoxin tolerance resulting in persistent inflammation thus contributing to septicemia and septic shock. We further report that this regulation is mediated by LPS-induced down-regulation of microRNAs 146a and 155. However, only over-expression of miR-146a, but not miR-155 abrogates morphine mediated hyper-inflammation, while antagonizing miR-146a (but not miR-155) augments morphine mediated hyper-inflammation. Hence, miR-146a could be the potential therapeutic target for morphine-mediated abrogation of endotoxin tolerance.
2013-08-01 | GSE42506 | GEO
Project description:Extracellular pH (pHe) is lower in many tumors than in the corresponding normal tissue. Acidic tumor microenvironment has been shown to facilitate epithelial mesenchymal transition (EMT) and tumor metastasis, while the mechanisms underlying tumor acidic microenvironment-induced tumor cell metastasis remain undefined. Here, we aimed to investigate the tumor metastasis and the EMT by acidic microenvironment and to explore their mechanisms and clinical significance in lung cancer. Results showed that acidic pHe remarkably enhanced invasion ability of lung cells accompanying with increased mesenchymal and decreased epithelial markers. Moreover, acidic pHe triggered the inhibition of microRNA-7 (miR-7) expression and activation of TGF-β2/SMAD signaling. Mechanistic studies showed that TGF-β2 is a direct potential target gene of miR-7, and acidity-induced metastasis could be abolished by treatment with a TGFβRI inhibitor, anti-TGF-β2 antibody and miR-7 mimic, respectively. The clinical samples further revealed that miR-7 was decreased in lung tissues and antagonistically correlated with TGF-β2 expression, associating with overall survival and metastasis. In conclusion, our study indicated that acidic pHe showed enhanced invasive potential, and enhanced potential to develop experimental metastases by a novel mechanism involving tumor acidic microenvironment-induced regulation of miR-7/TGF-β2/SMAD axis. Our findings suggest that the possibility that pHe of the primary tumor may be an important prognostic parameter for lung cancer patients merit clinical investigation. Moreover, miR-7 may serve as prognostic molecular marker and a novel therapeutic target for lung cancer.
2022-04-01 | PXD016524 | Pride
Project description:The colonization of distant organs by metastatic carcinoma cells underpins most human cancer-related deaths, including those from head and neck squamous cell carcinoma (HNSCC). We report that miR-203, a miRNA that promotes keratinocyte differentiation, is necessary and sufficient to inhibit multiple post-extravasation events during HNSCC lung metastasis, including initial survival/engraftment, escape from metastatic dormancy, and overt colonization in vivo. Restoration of miR-203 expression in established lung metastases reduces overall metastatic burden. Instead of promoting differentiation, miR-203 controls lung metastasis through direct targeting of genes involved in cytoskeletal dynamics (LASP1), ECM remodeling (SPARC), and cell metabolism (NUAK1). Expression of miR-203 and its downstream targets correlates with HNSCC overall survival outcomes, suggesting the therapeutic potential of targeting this signaling axis. Total RNA (including small RNAs) was isolated from cultured cells stably infected in biological duplicate with either a scrambled control hairpin or miR-203. Samples were harvested in technical duplicate.
2016-07-03 | E-GEOD-47028 | biostudies-arrayexpress
Project description:MiR-200c is a well-studied miRNA that is involved in stemness, the epithelial-mesenchymal transition, chemoresistance, radioresistance, and invasion/metastasis of various cancer cells. To obtain an overview of the lncRNA/mRNA regulated by miR-200c signaling in breast-cancer cell lines, we performed global lncRNA/mRNA-expression profiling on MDA-MB-231-pGIPZ and MDA-MB-231-miR-200c cells.
2018-08-28 | GSE119090 | GEO
Project description:Small cell lung cancer (SCLC) is the most lethal type of lung cancer, characterized by limited treatment options and rapid evolution from chemosensitivity to chemoresistance. However, the mechanisms underlying this evolution remain poorly understood. Identifying the druggable drivers and developing pharmacological strategies to overcome chemoresistance are imperative. Here, we show that Retinoid X receptor γ (RXRγ) is uniquely overexpressed in chemo-resistant SCLC tumors, and that RXRγ serves as an essential factor driving chemoresistance in SCLC. RXRγ forms phase-separated droplets with LSD1 in the nucleus, which enhances RXRγ-mediated gene transcription activity and reprograms gene expression, promoting tumor stemness and metastasis, and eventually driving SCLC chemoresistance. In turn, RXRγ antagonist disrupts RXRγ-LSD1 interaction, reducing their binding to the target gene locus, markedly suppressing the expression of the RXRγ target gene network. Finally, RXRγ antagonists strongly suppress tumor growth and metastasis and restore SCLC vulnerability to chemotherapy in multiple preclinical SCLC models, without overt toxicity, in mice. Thus, these results establish RXRγ as a key player in SCLC by phase separation and as a potential therapeutic target for this deadly disease.
2024-12-31 | GSE277738 | GEO
Project description:Small cell lung cancer (SCLC) is the most lethal type of lung cancer, characterized by limited treatment options and rapid evolution from chemosensitivity to chemoresistance. However, the mechanisms underlying this evolution remain poorly understood. Identifying the druggable drivers and developing pharmacological strategies to overcome chemoresistance are imperative. Here, we show that Retinoid X receptor γ (RXRγ) is uniquely overexpressed in chemo-resistant SCLC tumors, and that RXRγ serves as an essential factor driving chemoresistance in SCLC. RXRγ forms phase-separated droplets with LSD1 in the nucleus, which enhances RXRγ-mediated gene transcription activity and reprograms gene expression, promoting tumor stemness and metastasis, and eventually driving SCLC chemoresistance. In turn, RXRγ antagonist disrupts RXRγ-LSD1 interaction, reducing their binding to the target gene locus, markedly suppressing the expression of the RXRγ target gene network. Finally, RXRγ antagonists strongly suppress tumor growth and metastasis and restore SCLC vulnerability to chemotherapy in multiple preclinical SCLC models, without overt toxicity, in mice. Thus, these results establish RXRγ as a key player in SCLC by phase separation and as a potential therapeutic target for this deadly disease.
2024-12-31 | GSE268220 | GEO