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  • Title: Exosomal circ-AHCY promotes glioblastoma cell growth via Wnt/β-catenin signaling pathway.
    Author: Li Y, Zheng X, Wang J, Sun M, Li D, Wang Z, Li J, Li Y, Liu Y.
    Journal: Ann Clin Transl Neurol; 2023 Jun; 10(6):865-878. PubMed ID: 37150844.
    Abstract:
    BACKGROUND: Glioblastoma (GBM) is the most aggressive brain tumor. Reportedly, circular RNAs (circRNAs) participate in regulation of the development and progression of diverse cancers, including GBM. METHODS: Dysregulated circRNAs in GBM tissues were screened out from GEO database. The expression of candidate circRNAs in GBM cells was measured by qRT-PCR. Loss-of function assays, including colony formation assay, EdU assay, TUNEL assay, and flow cytometry analysis were conducted to determine the effects of circ-AHCY knockdown on GBM cell proliferation and apoptosis. Animal study was further used to prove the inhibitory effect of circ-AHCY silencing on GMB cell growth. Mechanistic experiments like luciferase reporter, RNA pull-down and RNA-binding protein immunoprecipitation (RIP) assays were performed to unveil the downstream molecular mechanism of circ-AHCY. Nanosight Nanoparticle Tracking Analysis (NTA) and PKH67 staining were applied to identify the existence of exosomes. RESULTS: Circ-AHCY was confirmed to be highly expressed in GBM cells. Circ-AHCY silencing suppressed GBM cell proliferation both in vitro and in vivo. Mechanistically, circ-AHCY activates Wnt/β-catenin signaling pathway by sequestering miR-1294 to up-regulate MYC which activated CTNNB1 transcription. It was also found that circ-AHCY recruited EIF4A3 to stabilize TCF4 mRNA. Enhanced levels of TCF4 and β-catenin contributed to the stability of TCF4/β-catenin complex. In turn, TCF4/β-catenin complex strengthened the transcriptional activity of circ-AHCY. Exosomal circ-AHCY derived from GBM cells induced abnormal proliferation of normal human astrocytes (NHAs). CONCLUSION: Exosomal circ-AHCY forms a positive feedback loop with Wnt/β-catenin signaling pathway to promote GBM cell growth.
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