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Keywords {🔍}

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Topics {✒️}

n6-methyladenosine-dependent post-transcriptional modification regulating mir-30c-2-3p/akt1s1 axis prl-tk-pmir-fto 3’utr zeb1 activated-vps9d1-as1 promotes m6a-hur-dependent epigenetic silencing prl-tk-pmir-circgpr137b 3’utr empty vector plv-circ-luci regulating mir-548p/pbld axis targeting mir-194-5p/foxa1 axis rna n6-methyladenosine methyltransferase mir-367-5p/p27 kip1 axis promotes oxidored-nitro domain protein-coupled receptor 137b circgpr137b/mir-4739/fto feedback loop n-methyladenosine rna demethylase article download pdf lncrna mcm3ap-as1 promotes analysis software image-pro sponge mir-516a-5p/− 326/− 532-5p digoxin-labeled probe sequence biotin-labeled probe sequence quantitative real-time pcr mettl14-mediated m6a modification ythdf2-dependent posttranscriptional silencing circ-cdyl acts specifically dual-luciferase reporter assay fto-mediated m6a modification n6-methyladenosine modification full size image plv-sh-circgpr137b/sh-nc m6a-dependent modifications [31 regulating β-catenin signaling hepatocellular carcinoma metastasis sk-hep-1 cell line dual-luciferase reporter assays sponging mir-516a-5p mediated m6a demethylation exosome-mediated secretion circrna-100338/mir-141-3p pathway sk-hep-1 xenograft tumors common rna modifications hsa_circ_0072309 promotes tumorigenesis zhong shan hospital kaplan–meier analysis revealed sponging mir-4739/fto axis engineering circular rna luciferase-labeled hepg2 cells stem cell res positive feedback loop n6-methyladenosine mettl3/14/16

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         headline:CircGPR137B/miR-4739/FTO feedback loop suppresses tumorigenesis and metastasis of hepatocellular carcinoma
         description:Emerging evidence indicates that circular RNAs (circRNAs) and m6A RNA methylation participate in the pathogenesis and metastasis of multiple malignancies including hepatocellular carcinoma (HCC). However, it remains undocumented how circRNAs form a feedback loop with the m6A modification contributing to HCC. A novel hsa_circ_0017114 (circGPR137B) was identified from three pairs of primary HCC and adjacent normal tissues by circRNA expression profiling. The association of circGPR137B and miR-4739 with clinicopathological parameters and prognosis in patients with HCC was analyzed by RT-qPCR, fluorescence in situ hybridization and TCGA cohorts. The role of circGPR137B in HCC was estimated in vitro and in vivo. RT-qPCR, western blot, m6A dot blot, RIP, MeRIP and dual-luciferase reporter assays were used to validate the reciprocal regulation of the feedback loop among circGPR137B, miR-4739 and m6A demethylase FTO. Meanwhile, the expression, function and prognosis of FTO in HCC were investigated by RT-qPCR, western blot, TCGA and rescue experiments. We identified a new dramatically downregulated circGPR137B in HCC tissues, and found that downregulation of circGPR137B or upregulation of miR-4739 was associated with poor prognosis in patients with HCC. Ectopic expression of circGPR137B strikingly repressed the proliferation, colony formation and invasion, whereas knockdown of circGPR137B harbored the opposite effects. Moreover, restored expression of circGPR137B inhibited tumor growth and lung metastasis in vivo. Further investigations showed that circGPR137B, co-localized with miR-4739 in the cytoplasm, acted as a sponge for miR-4739 to upregulate its target FTO, which mediated m6A demethylation of circGPR137B and promoted its expression. Thus, a feedback loop comprising circGPR137B/miR-4739/FTO axis was formed. FTO suppressed cell growth and indicated favorable survival in patients with HCC. Our results demonstrate that circGPR137B inhibits HCC tumorigenesis and metastasis through the circGPR137B/miR-4739/FTO feedback loop. This positive feedback mechanism executed by functional coupling between a circRNA sponge and an m6A modification event suggests a model for epigenetics.
         datePublished:2022-07-20T00:00:00Z
         dateModified:2022-07-20T00:00:00Z
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            miR-4739
            m6A
            Demethylation
            Hepatocellular carcinoma
            FTO
            Cancer Research
            Oncology
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      headline:CircGPR137B/miR-4739/FTO feedback loop suppresses tumorigenesis and metastasis of hepatocellular carcinoma
      description:Emerging evidence indicates that circular RNAs (circRNAs) and m6A RNA methylation participate in the pathogenesis and metastasis of multiple malignancies including hepatocellular carcinoma (HCC). However, it remains undocumented how circRNAs form a feedback loop with the m6A modification contributing to HCC. A novel hsa_circ_0017114 (circGPR137B) was identified from three pairs of primary HCC and adjacent normal tissues by circRNA expression profiling. The association of circGPR137B and miR-4739 with clinicopathological parameters and prognosis in patients with HCC was analyzed by RT-qPCR, fluorescence in situ hybridization and TCGA cohorts. The role of circGPR137B in HCC was estimated in vitro and in vivo. RT-qPCR, western blot, m6A dot blot, RIP, MeRIP and dual-luciferase reporter assays were used to validate the reciprocal regulation of the feedback loop among circGPR137B, miR-4739 and m6A demethylase FTO. Meanwhile, the expression, function and prognosis of FTO in HCC were investigated by RT-qPCR, western blot, TCGA and rescue experiments. We identified a new dramatically downregulated circGPR137B in HCC tissues, and found that downregulation of circGPR137B or upregulation of miR-4739 was associated with poor prognosis in patients with HCC. Ectopic expression of circGPR137B strikingly repressed the proliferation, colony formation and invasion, whereas knockdown of circGPR137B harbored the opposite effects. Moreover, restored expression of circGPR137B inhibited tumor growth and lung metastasis in vivo. Further investigations showed that circGPR137B, co-localized with miR-4739 in the cytoplasm, acted as a sponge for miR-4739 to upregulate its target FTO, which mediated m6A demethylation of circGPR137B and promoted its expression. Thus, a feedback loop comprising circGPR137B/miR-4739/FTO axis was formed. FTO suppressed cell growth and indicated favorable survival in patients with HCC. Our results demonstrate that circGPR137B inhibits HCC tumorigenesis and metastasis through the circGPR137B/miR-4739/FTO feedback loop. This positive feedback mechanism executed by functional coupling between a circRNA sponge and an m6A modification event suggests a model for epigenetics.
      datePublished:2022-07-20T00:00:00Z
      dateModified:2022-07-20T00:00:00Z
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         CircGPR137B
         miR-4739
         m6A
         Demethylation
         Hepatocellular carcinoma
         FTO
         Cancer Research
         Oncology
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