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MiR-192-EGR1/HOXB9 regulatory network controls the angiogenic switch in cancer.

ABSTRACT: A deeper mechanistic understanding of tumor angiogenesis regulation is needed to improve current anti-angiogenic therapies, which thus far have only modestly improved patient survival. We present converging evidence from systems-based miRNA analyses of large-scale patient datasets along with in vitro and in vivo experiments that identify miR-192 as a key regulator of angiogenesis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69990 | GEO | 2016/03/21

SECONDARY ACCESSION(S): PRJNA287354

REPOSITORIES: GEO

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A miR-192-EGR1-HOXB9 regulatory network controls the angiogenic switch in cancer.

Project description:A deeper mechanistic understanding of tumour angiogenesis regulation is needed to improve current anti-angiogenic therapies. Here we present evidence from systems-based miRNA analyses of large-scale patient data sets along with in vitro and in vivo experiments that miR-192 is a key regulator of angiogenesis. The potent anti-angiogenic effect of miR-192 stems from its ability to globally downregulate angiogenic pathways in cancer cells through regulation of EGR1 and HOXB9. Low miR-192 expression in human tumours is predictive of poor clinical outcome in several cancer types. Using 1,2-dioleoyl-sn-glycero-3-phosphatidylcholine (DOPC) nanoliposomes, we show that miR-192 delivery leads to inhibition of tumour angiogenesis in multiple ovarian and renal tumour models, resulting in tumour regression and growth inhibition. This anti-angiogenic and anti-tumour effect is more robust than that observed with an anti-VEGF antibody. Collectively, these data identify miR-192 as a central node in tumour angiogenesis and support the use of miR-192 in an anti-angiogenesis therapy.

| S-EPMC4822037 | biostudies-literature

Expression data from Arabidopsis wild-type, sicy-192, and sicy-192 gun1-101 plants

Project description:Plastid gene expression (PGE) acts as a signal that regulates the expression of photosynthesis-associated nuclear genes (PhANGs) via GENOMES UNCOUPLED1 (GUN1)-dependent retrograde signaling. We recently isolated Arabidopsis sugar-inducible cotyledon yellow-192 (sicy-192), a gain-of-function mutant of plastidic invertase (INV-E), and showed that following the treatment of this mutant with sucrose, the expression of PhANGs decreased while that of nitrate reductase 1 (NIA1) increased. Plastid-encoded RNA polymerase (PEP)-dependent PGE was markedly suppressed in the sicy-192 mutant by the sucrose treatment. A double mutant of sicy-192 and gun1-101, a null mutant of GUN1, revealed that metabolic perturbation in the sucrose-treated sicy-192 mutant was, at least in part, dependent on GUN1. To confirm whether there is a relationship between plastid sugar metabolism and nuclear gene expression, we performed a microarray analysis using Suc-treated 3 genotypes consisting of wild-type, sicy-192, and sicy-192 gun1-101 plants.

2013-09-14 | GSE50857 | GEO

The angiogenic switch leads to a metabolic shift in human glioblastoma

Project description:The gene expression profiles of two groups of triplicate human glioblastoma (GBM) xenografts grown in immunodeficient rats were compared. The first group of xenografts was derived from a patient biopsy with Epidermal Growth Factor Receptor (EGFR) amplification which grows highly invasive and is independent of angiogenesis. The second group was obtained by introducing a dominant-negative EGFR mutant into the tumor cells, leading to a progression of the tumors to an angiogenic phenotype associated with a transition from a proneural to a mesenchymal GBM molecular subtype.

2017-07-05 | E-MTAB-4898 | biostudies-arrayexpress

Expression data from Arabidopsis wild-type, sicy-192, and sicy-192 gun1-101 plants

2013-09-14 | E-GEOD-50857 | biostudies-arrayexpress

Sinorhizobium fredii strain:USDA 192 | isolate:USDA 192

Project description:Sinorhizobium fredii USDA 192 genome sequencing

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Gene expression profiling of the tumor angiogenic switch in Rip1Tag2 mice

Project description:Angiogenesis represents a rate-limiting step during tumor progression. Molecular mechanisms driving tumor angiogenesis (e.g. implicating signaling by VEGFs and their receptors) have been elucidated and allowed to design targeted therapies. However, limits of such anti-angiogenic therapies have emerged, notably because tumor cells adapt and tumors recur in more aggressive fashions. There is therefore a need to identify novel mechanisms implicated in tumor angiogenesis that have a potential towards translational applications. Using a transgenic murine model of pancreatic neuroendocrine cancer (Hanahan, Nature 315, 1985) where angiogenesis represents an early and discrete step of multi-stage tumor progression (Folkman et al. , Nature 339, 1989), we compared non-angiogenic and angiogenic early tumors to obtain a comprehensive description of the tumor angiogenic switch at the level of gene expression.

2015-01-01 | GSE51637 | GEO

Paenibacillus sp. BR1-192

Project description:Paenibacillus sp. BR1-192 Genome sequencing

| PRJNA941370 | ENA

Kluyvera ascorbata strain:192

Project description:Kluyvera ascorbata strain:192 Genome sequencing

| PRJNA1158828 | ENA

Lentinula edodes strain:12P103(192)

Project description:Lentinula edodes 12P103(192) QTL resequencing

| PRJNA871663 | ENA

Coordinated regulation of cell cycle transcripts by p53-inducible microRNAs, miR -192 and -215

Project description:Cell cycle arrest in response to DNA damage is an important anti-tumorigenic mechanism. microRNAs (miRNAs) were shown recently to play key regulatory roles in cell cycle progression. For example, miR-34a is induced in response to p53 activation and mediates G1 arrest by down-regulating multiple cell cycle-related transcripts. Here we show that genotoxic stress promotes the p53-dependent up-regulation of the homologous miRNAs, miR -192 and miR-215. Like miR-34a, activation of miR-192/215 induces cell cycle arrest suggesting that multiple microRNA families operate in the p53 network. Furthermore, we define a downstream gene expression signature for miR-192/215 expression that includes a number of transcripts that regulate G1 and G2 checkpoints. Of these transcripts, 18 transcripts are direct targets of miR-192/215 and the observed cell cycle arrest likely results from a cooperative effect among the modulations of these genes by the miRNAs. Our results demonstrating a role for miR-192/215 in cell proliferation combined with recent observations that these miRNAs are under-expressed in primary cancers support the idea that miR-192 and miR-215 function as tumor-suppressors.

2008-12-07 | GSE13105 | GEO

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