Show pageBacklinksCite current pageExport to PDFBack to top This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong. ====== Adenosylhomocysteinase ====== Dysregulated [[circRNA]]s in GBM tissues were screened out from [[Gene Expression Omnibus]] database. The expression of candidate circRNAs in GBM cells was measured by qRT-PCR. [[Loss-of-function assay]]s, 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) ((Li Y, Zheng X, Wang J, Sun M, Li D, Wang Z, Li J, Li Y, Liu Y. Exosomal circ-AHCY promotes glioblastoma cell growth via Wnt/β-catenin signaling pathway. Ann Clin Transl Neurol. 2023 May 7. doi: 10.1002/acn3.51743. Epub ahead of print. PMID: 37150844.)). adenosylhomocysteinase.txt Last modified: 2024/06/07 02:50by 127.0.0.1