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CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation

ABSTRACT: CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation

PROVIDER: PRJNA698359 | ENA |

REPOSITORIES: ENA

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CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation

Project description:High-grade glioma is highly aggressive and malignant, resistant to combined therapies and easy to relapse. A better understanding of circRNA biological function in high-grade glioma might contribute to the therapeutic efficacy. Here, a circRNA merely up-regulated in high-grade glioma, circGLIS3 (hsa_circ_0002874, originating from exon 2 of GLIS3), was validated by microarray and qRT-PCR. Functional experiments uncovered that up-regulation of circGLIS3 promoted glioma cell migration and invasion, and showed aggressive characteristics in tumor-bearing mice. Fluorescence in situ hybridization, RNA pull-down, RNA immunoprecipitation and immunohistochemical staining showed that circGLIS3 could promoted Ezrin T567 phosphorylation. Further investigation showed that circGLIS3 could be excreted by glioma through exosomes and induced endothelial cells angiogenesis. This study indicates that circGLIS3 is up-regulated in high-grade glioma and contributes to the invasion and angiogenesis of glioma via promoting Ezrin T567 phosphorylation.

2021-09-22 | GSE165859 | GEO

CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation (microarray)

Project description:CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation (microarray)

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CircGLIS3 promotes high-grade glioma invasion via modulating Ezrin phosphorylation (microarray)

2021-09-22 | GSE165926 | GEO

CircGLIS3 Promotes High-Grade Glioma Invasion via Modulating Ezrin Phosphorylation.

Project description: Not available

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Oxidative phosphorylation promotes primary melanoma invasion

Project description:Oxidative phosphorylation promotes primary melanoma invasion

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Oxidative phosphorylation promotes primary melanoma invasion

Project description:Dermal invasion is a hallmark of malignant melanoma. The molecular alterations driving the progression of primary melanoma to metastatic disease have been studied extensively, whereas the early progression of non-invasive primary melanoma to an invasive state is not well understood. To elucidate the mechanisms underlying the transition from radial to vertical growth, the first step in melanoma invasion, we developed a zebrafish melanoma model in which constitutive activation of ribosomal protein S6 kinase 1 (RSK1) drives tumor invasion. Transcriptomic analysis of RSK1-activated tumors identified metabolic changes, including upregulation of genes associated with oxidative phosphorylation. Vertical growth phase human melanoma cells show higher oxygen consumption and preferential utilization of glutamine compared to radial growth phase melanoma cells. Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC1a has been proposed as a master regulator of tumor oxidative phosphorylation. In human primary melanoma specimens we show that PGC1a protein expression is positively associated with increased tumor thickness and expression of the proliferative marker Ki-67 and the reactive oxygen species (ROS) scavenger SCARA3. PGC1a depletion modulates cellular processes associated with primary melanoma growth and invasion, including oxidative stress. Our results support a role for PGC1a in mediating glutamine-driven OXPHOS to facilitate the invasive growth of primary melanoma.

2020-01-24 | GSE144117 | GEO

circZFR promote lung carcinogenesis and oxidative phosphorylation by modulating alternative splicing

Project description:circZFR promote lung carcinogenesis and oxidative phosphorylation by modulating alternative splicing

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PLD1 promotes tumor invasion by regulation of MMP-13 expression via phosphorylation of NF-kB in bladder cancer

Project description:Invasion of bladder cancer (BC) cells from the mucosa into the muscle layer is canonical for BC progression while phospholipase D isoform 1 (PLD1) is known to mediate development of cancer through phosphatidic acid (PA) production. We therefore used in silico, in vitro and in vivo approaches to detail the effect of PLD1 on BC invasion. In BC patients, higher levels of PLD1 expression were associated with poor prognosis. PLD1 knockdown significantly suppressed cellular invasion by human BC cells and matrix metalloproteinase-13 (MMP-13) was observed to be an invasion mediator gene. In our mouse bladder carcinogenesis model, the development of invasive BCs was suppressed by PLD1 knockout and a global transcriptomic analysis in this model indicated MMP-13 as a potential tumor invasion gene with NF-kB (nuclear factor-kB) as its transcription regulator. Furthermore, PA administration increased both MMP-13 expression and NF-kB p65 phosphorylation levels. Collectively, we demonstrate that PLD1 promotes tumor invasion of BC by regulation of MMP-13 expression via phosphorylation of NF-kB p65. Our results suggest that PLD1 is a potential therapeutic target to prevent progression in BC patients.

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Transcription profiling of human tumors of breast cancer 129 patients were analyzed for the ability to predict biomarkers (ER, PR, HER2), histologic features (grade and lymphatic-vascular invasion), and stage-related information (tumor size and lymph node metastasis)

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