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CircRNA circBACH1 facilitates hepatitis B virus replication and hepatoma development by regulating the miR-200a-3p/MAP3K2 axis

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dc.contributor.authorDu, Na
dc.contributor.authorLi, Kailin
dc.contributor.authorWang, Yu
dc.contributor.authorSong, Bo
dc.contributor.authorZhou, Xuan
dc.contributor.authorDuan, Shaoqiong
dc.date.accessioned2023-03-01T09:23:56Z
dc.date.available2023-03-01T09:23:56Z
dc.date.issued2022
dc.description.abstractBackground. Hepatitis B virus (HBV) is a top contributor to hepatoma. Circular RNAs (circRNAs) have been elucidated to have a close connection with HBV-induced hepatoma. This study aimed to explore the role of circRNA BTB domain and CNC homolog 1 (circBACH1) in HBV replication and hepatoma progression, as well as the potential mechanistic pathway. Methods. Quantitative real-time polymerase chain reaction (qRT-PCR) assay was performed to assess the expression of circBACH1, microRNA (miR)-200a-3p, and mitogen-activated protein kinase kinase kinase 2 (MAP3K2). HBV replication was determined by enzyme-linked immunosorbent assay (ELISA) and qRTPCR assay. Cell viability and clonogenicity were detected via Cell Counting Kit-8 (CCK-8) assay and colony formation assay, respectively. Cell metastasis was examined by Transwell assay and wound healing assay. Annexing-V/PI staining was employed to monitor cell apoptosis using flow cytometry. Levels of MAP3K2, proliferation- and apoptosis-related proteins were analyzed by Western blotting. Target interaction between miR-200a-3p and circBACH1 or MAP3K2 was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The role of circBACH1 in vivo was investigated by xenograft model assay. Results. Expression of circBACH1 and MAP3K2 was increased, while miR-200a-3p expression was decreased in HCC tissues and HBV-transfected hepatoma cells. Depletion of circBACH1 or miR-200a3p overexpression impeded HBV replication, proliferation, and metastasis in HBV-transfected hepatoma cells. CircBACH1 was able to regulate MAP3K2 expression by sponging miR-200a-3p. CircBACH1 regulated HBV replication and hepatoma progression through the miR-200a-3p/MAP3K2 pathway. Moreover, circBACH1 deficiency hampered tumor growth in vivo. Conclusion. CircBACH1 knockdown had inhibitory effects on HBV replication and hepatoma progression, at least partly by modulating the miR-200a-3p/MAP3K2 axises
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dc.format.extent15es
dc.identifier.citationHistology and Histopathology Vol. 37, nº9 (2022)
dc.identifier.doihttps://doi.org/ 10.14670/HH-18-452
dc.identifier.issn0213-3911
dc.identifier.issn1699-5848
dc.identifier.urihttp://hdl.handle.net/10201/128908
dc.languageenges
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histiologiaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectHepatomaes
dc.subjectHBV replicationes
dc.subjectcircBACH1es
dc.subjectmiR-200a-3pes
dc.subjectMAP3K2es
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleCircRNA circBACH1 facilitates hepatitis B virus replication and hepatoma development by regulating the miR-200a-3p/MAP3K2 axises
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.37, nº9 (2022)