Publication: CircRNA circBACH1 facilitates hepatitis B virus replication and hepatoma development by regulating the miR-200a-3p/MAP3K2 axis
Authors
Du, Na ; Li, Kailin ; Wang, Yu ; Song, Bo ; Zhou, Xuan ; Duan, Shaoqiong
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/ 10.14670/HH-18-452
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info:eu-repo/semantics/article
Description
Abstract
Background. 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
axis
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