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Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer [mRNA]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE67728 | GEO | 2015/04/10

SECONDARY ACCESSION(S): PRJNA280763

REPOSITORIES: GEO

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Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer [mRNA]

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

Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer [miRNA]

Project description:This experiment is designed to screen miRNAs that are deregulated during chemoresistance-associated metastasis of lung cancer cells. Chemoresistant metastatic in vivo tumor model of A549-luc-Vector cells was established after four rounds of cisplatin (CDDP) treatments compared to corresponding control solvent treatments. Upon examining profiles of miRNA expression differential between tumor-derived cultured cells from the Ctrl-4th and CDDP-4th treatments, most markedly upregulated and downregulated miRNAs in chemoresistant, metastatic A549-luc-CDDP-4th cells were identified. In order to establish a chemoresistant in vivo tumor model, after inoculation of A549-luc-Vector cells, cisplatin (CDDP) or control solvent was intraperitoneally (i.p.) injected six rounds in a two-week period and cells were isolated from corresponding resultant tumors, cultured and re-transplanted into syngeneic mice to receive the next round of treatment. In our experimental model, human lung cancer xenografts developed chemoresistance in the third round of CDDP treatment (CDDP-3rd) and chemoresistance-associated metastases following the fourth round of treatment. Tumor-derived cultured cells from Ctrl-4th and CDDP (cisplatin)-4th treatment were subjected to miRNA array (Agilent-031181 human miRNA (8*60k) V16.0) analysis, with two biological replications for each treatment.

2015-04-10 | E-GEOD-67727 | biostudies-arrayexpress

Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer [miRNA]

2015-04-10 | GSE67727 | GEO

Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-04-10 | E-GEOD-67729 | biostudies-arrayexpress

Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer

Project description:Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer

| PRJNA280760 | ENA

Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-04-10 | GSE67729 | GEO

Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [miRNA-seq]

Project description:To identify the potential microRNAs (miRNAs) involved in the regulation of cardiomyocyte (CM) proliferation during homeostasis and injury, RNA sequencing (RNA-seq) in mouse cardiac ventricles was performed on postnatal day 1, 7, and 28 (P1, P7, and P28). Significant upregulation of MiR-128 was found in P7 hearts as compared to P1. To further specify the effect of miR-128 in the heart, RNA-Seq was performed in control mice (Ctrl) and miR-128 overexpression mice (miR-128OE) on P7. These data provide novel insights into the mechanisms by which adult CMs exit the cell cycle arrest and is fundamental for therapeutic manipulation to stimulate endogenous CM proliferate in cardiac regeneration.

2018-01-02 | GSE107679 | GEO

Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [RNA-seq]

2018-01-02 | GSE107678 | GEO

Astroglial FMRP deficiency cell-autonomously up-regulates miR-128 and disrupts developmental astroglial mGluR5 signaling (miRNA)

Project description:The loss of fragile X mental retardation protein (FMRP) causes fragile X syndrome (FXS), the most common inherited intellectual disability. How the loss of FMRP alters protein expression and astroglial functions remains essentially unknown. Here we showed that selective loss of astroglial FMRP in vivo up-regulates a brain-enriched miRNA, miR-128-3p, in mouse and human FMRP-deficient astroglia, which suppresses developmental expression of astroglial metabotropic glutamate receptor 5 (mGluR5), a major receptor in mediating developmental astroglia to neuron communication. Selective in vivo inhibition of miR-128-3p in FMRP-deficient astroglia sufficiently rescues decreased mGluR5 function, while astroglial overexpression of miR-128-3p strongly and selectively diminishes developmental astroglial mGluR5 signaling. Subsequent transcriptome and proteome profiling further suggests that FMRP commonly and preferentially regulates protein expression through posttranscriptional, but not transcriptional, mechanisms in astroglia. Overall, our study defines an FMRP-dependent cell-autonomous miR pathway that selectively alters developmental astroglial mGluR5 signaling, unveiling astroglial molecular mechanisms involved in FXS pathogenesis.

2020-09-10 | GSE157724 | GEO

Differentially expressed genes and transcript isoforms in mouse NSCs expressing miR-128

Project description:We identify a brain-specific microRNA—miR-128—that represses Nonsense Mediated mRNA Decay (NMD) and thereby controls batteries of transcripts in neural cells. miR-128 represses NMD by targeting the RNA helicase UPF1 and the exon-junction complex core component MLN51. We employed exon arrays for this analysis, as this platform detects expression levels of individual exons and thus allows detection of not only differentially expressed transcripts (DETs), but also alternative isoform transcripts (AITs). The latter is particularly relevant to our study because alternative RNA processing events (e.g., RNA splicing, alternative promoter usage, and alternative polyadenylation-site usage) often place a translation termination codon in a premature context and thereby trigger NMD. Compare different expressed genes and transcript isoforms in mouse NSCs miR-128 positive vs miR-128 negative (Control). Mouse NSCs, that do not normally express miR-128, were nucleofected with either miR-128 (biological triplicates were analysed) or miR-Control (biological triplicates). RNA was extracted 72hrs later, and Exon Array was performed to identify target genes.

2011-04-28 | E-GEOD-28889 | biostudies-arrayexpress

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