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The long noncoding RNA H19 regulates tumor plasticity in neuroendocrine prostate cancer [ChIP-seq]

ABSTRACT: The long noncoding RNA H19 regulates tumor plasticity in neuroendocrine prostate cancer [ChIP-seq]

PROVIDER: PRJNA762568 | ENA |

REPOSITORIES: ENA

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The long noncoding RNA H19 regulates tumor plasticity in neuroendocrine prostate cancer

Project description:The long noncoding RNA H19 regulates tumor plasticity in neuroendocrine prostate cancer

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The long noncoding RNA H19 regulates tumor plasticity in neuroendocrine prostate cancer [ChIP-seq]

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The long noncoding RNA H19 regulates tumor plasticity in neuroendocrine prostate cancer

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The long noncoding RNA H19 regulates tumor plasticity in neuroendocrine prostate cancer.

Project description: Not available

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Identification of genes regulated by long noncoding RNA H19 in the ovary.

Project description:In order to identify genes regulated by long noncoding RNA H19 in the ovary, we performed RNA-Seq with WT and H19KO ovaries from 8-week old mice. Among the differentially expressed genes, we found anti-mullerian hormone (AMH), which potentially plays an important role in regulating ovarian follicular development, might be a target of H19 mediated regulation.

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Identification of genes regulated by long noncoding RNA H19 in skeletal muscle

Project description:Soleus muscle has the most abundant H19 expression compared to other skeletal muscle tissues. In order to identify genes regulated by long noncoding RNA H19 in skeletal muscle, we performed RNA-Seq with dissected WT and H19KO soleus muscles from 21 week old mice. Among the differentially expressed genes, we found skeletal muscle - overexpressed gene DUSP27, which potentially plays an important role in regulating skeletal muscle glucose metabolisim by regulating the activitiy of AMPK, might be a target of H19 mediated regulation.

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Identification of genes regulated by Long noncoding RNA H19 in hepatic cells

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DPYSL5 is Highly Expressed in treatment-induced Neuroendocrine Prostate Cancer and Promotes Lineage Plasticity via EZH2/PRC2

Project description:Treatment-induced neuroendocrine prostate cancer (t-NEPC) is a lethal subtype of castration-resistant prostate cancer resistant to androgen receptor (AR) inhibitors. Our study unveils that AR suppresses neuronal development protein dihydropyrimidinase-related protein 5 (DPYSL5), providing a mechanism for neuroendocrine transformation under androgen deprivation therapy. Our unique CRPC-NEPC cohort with 157 patient samples, including 55 t-NEPC patient samples, shows a high expression of DPYSL5 in t-NEPC patients, and that DPYSL5 correlates with neuroendocrine markers and inversely with AR and PSA. DPYSL5 overexpression in prostate cancer cells induces neuron like phenotype, enhances invasion, proliferation, and upregulates stemness and neuroendocrine related markers. Mechanistically, DPYSL5 promotes prostate cancer cell plasticity via EZH2-mediated PRC2 activation. Depletion of DPYSL5 halts proliferation, induces G1 phase cell cycle arrest, reverses neuroendocrine phenotype and upregulates luminal genes. In conclusion, DPYSL5 plays a critical role in regulating prostate cancer cell plasticity, and we propose the AR/DPYSL5/EZH2/PRC2 axis as a novel driver of t-NEPC progression.

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Protein Identification and Post-translational Analysis of DMD and its associated Proteins in H19-proficient and -deficient Cells

Project description:Dystrophin proteomic regulation in Muscular Dystrophies (MD) remains unclear. We report that a long noncoding RNA (lncRNA) H19 associates with dystrophin. To investigate the biological roles of this interaction in vivo, we performed mass spectrometry analysis of dystrophin and its associated proteins in H19-proficient and -deficient C2C12 myotubes. Mass spectrometry data indicated that in H19-proficient myotubes, dystrophin associates with components of dystrophin-associated protein complex (DPC); however, in H19-deficient myotubes, dystrophin associated with UBA1, UB2G1, TRIM63 ubiquitin E3 ligase and ubiquitin. In H19-deficient myotubes, dystrophin was post-translationally modified with K48-linked poly-ubiquitination at Lys3577 (referred to as Ub-DMD). This mass spectrometry study demonstrated that lncRNA H19, associates with dystrophin and inhibits E3 ligase-dependent Ub-DMD formation and its subsequent proteasomal degradation. Based on this study, H19 RNA oligonucleotides conjugated with a muscle homing ligand Agrin (referred to as AGR-H19) and Nifenazone, a TRIM63-specific small molecule inhibitor, reverses the dystrophin degradation in iPSC-derived skeletal muscle cells from Becker Muscular Dystrophy patients. Furthermore,treatment of mdx mice with exon-skipping reagent, in combination with either AGR-H19 or Nifenazone, dramatically stablized dystrophin, preserved skeletal/cardiac muscle histology, and improved strength/heart function. In summary, this mass spectrometry study paves the way to meaningful targeted therapeutics for BMD and certain DMD patients.

2020-08-19 | PXD020566 | Pride

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