ror2 和 lincrna cox2-ror相同吗

OnlineFirst | Molecular Cancer Research
March 09, 2018
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Mol Cancer Res DOI:10.86.MCR-17-0230Extracellular vesicle-mediated transfer of long non-coding RNA ROR modulates chemosensitivity in human hepatocellular cancer - ScienceDirect
Download PDFDownloadExport JavaScript is disabled on your browser. Please enable JavaScript to use all the features on this page., 2014, Pages 458-467open accessAuthor links open overlay panelShow moreHighlightsoSelected long non-coding RNA are aberrantly expressed in hepatocellular cancers.olinc-ROR is a highly upregulated lncRNA that is expressed in response to TGFβ.olinc-ROR contributes to chemoresistance of HCC cells.oIntercellular transfer of linc-ROR occurs within extracellular vesicles.AbstractHepatocellular cancers (HCC) are highly resistant to chemotherapy. TGFβ has been associated with chemoresistance in some human cancers but the mechanisms involved are unknown. We explored how TGFβ might contribute to altered responses to therapy by assessing the involvement and mechanistic contribution of extracellular vesicle long non-coding RNA (lncRNA) in mediating TGFβ-dependent chemoresistance. TGFβ reduced the sensitivity of HCC cells to sorafenib or doxorubicin and altered the release of both extracellular vesicles and of selected lncRNA within these vesicles. Amongst these, lincRNA-ROR (linc-ROR), a stress-responsive lncRNA was highly expressed in HCC cells and enriched within extracellular vesicles derived from tumor cells. Incubation with HCC-derived extracellular vesicles increased linc-ROR expression and reduced chemotherapy-induced cell death in recipient cells. Sorafenib increased linc-ROR expression in both tumor cells and extracellular vesicles, whereas siRNA to linc-ROR increased chemotherapy-induced apoptosis and cytotoxicity. Tumor-initiating cells that express CD133 have an increased resistance to therapy. TGFβ increased expression of CD133+ cells and colony growth in limiting dilution assays, both of which were attenuated by linc-ROR knockdown. These data provide mechanistic insights into primary chemoresistance in HCC by showing that: (a) TGFβ selectively enriches linc-RoR within extracellular vesicles, which has a potential role in intercellular signaling in response to TGFβ; (b) expression and enrichment of linc-ROR during chemotherapeutic stress plays a functional rol and (c) the effects of TGFβ on chemoresistance in HCC may involve linc-RoR-dependent effects on tumor-initiating cells. These findings implicate extracellular vesicle lncRNA as mediators of the chemotherapeutic response, and support targeting linc-ROR to enhance chemosensitivity in HCC.AbbreviationsEVextracellular vesicleHCChepatocellular carcinomamiRNAmicroRNAVDvesicle-depletedlncRNAlong non-coding RNAlinc-RORlong intergenic non-coding RNATGFβtransforming growth factor βCTcycle thresholdsiRNAsmall interfering RNAKeywordsLiver cancerChemoresistanceExosomesGene expressionRNA genesRecommended articlesCiting articles (0)The Imprinted H19 LncRNA Antagonizes Let-7 MicroRNAs - ScienceDirect
Download PDFDownloadExport JavaScript is disabled on your browser. Please enable JavaScript to use all the features on this page., 10 October 2013, Pages 101-112Author links open overlay panelShow moreopen archiveHighlightsoH19 lncRNA harbors both canonical and noncanonical binding sites for let-7 microRNAsoH19 lncRNA acts as a natural sponge for let-7oH19 depletion causes accelerated muscle differentiation in vitroSummaryAbundantly expressed in fetal tissues and adult muscle, the developmentally regulated H19 long noncoding RNA (lncRNA) has been implicated in human genetic disorders and cancer. However, how H19 acts to regulate gene function has remained enigmatic, despite the recent implication of its encoded miR-675 in limiting placental growth. We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.Recommended articlesCiting articles (0)Endogenous miRNA Sponge lincRNA-RoR Regulates Oct4, Nanog, and Sox2 in Human Embryonic Stem Cell Self-Renewal - ScienceDirect
Download PDFDownloadExport JavaScript is disabled on your browser. Please enable JavaScript to use all the features on this page., 15 April 2013, Pages 69-80Author links open overlay panelShow moreopen archiveSummaryThe embryonic stem cell (ESC) transcriptional and epigenetic networks are controlled by a multilayer regulatory circuitry, including core transcription factors (TFs), posttranscriptional modifier microRNAs (miRNAs), and some other regulators. However, the role of large intergenic noncoding RNAs (lincRNAs) in this regulatory circuitry and their underlying mechanism remains undefined. Here, we demonstrate that a lincRNA, linc-RoR, may function as a key competing endogenous RNA to link the network of miRNAs and core TFs, e.g., Oct4, Sox2, and Nanog. We show that linc-RoR shares miRNA-response elements with these core TFs and that linc-RoR prevents these core TFs from miRNA-mediated suppression in self-renewing human ESC. We suggest that linc-RoR forms a feedback loop with core TFs and miRNAs to regulate ESC maintenance and differentiation. These results may provide insights into the functional interactions of the components of genetic networks during development and may lead to new therapies for many diseases.Graphical AbstractHighlights? A lincRNA-RoR function as a key competing endogenous RNA in hESCs ? Linc-RoR prevents core TFs from microRNA-mediated suppression ? Linc-RoR forms a feedback loop with core TFs and microRNAs ? Linc-RoR is a key regulator of hESC self-renewal and differentiationRecommended articlesCiting articles (0)

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