Abstract
Circular RNAs (circRNAs) are newly classified noncoding RNA (ncRNA) members with a covalently closed continuous loop structure that are involved in immune responses against hepatitis B virus (HBV) infections and play important biological roles in the occurrence and pathogenesis of HCC progression. The roles of circRNAs in HBV-associated HCC (HBV-HCC) have gained increasing attention. Substantial evidence has revealed that both tissue and circulating circRNAs may serve as potential biomarkers for diagnostic, prognostic and therapeutic purposes. So far, at least four circRNA/miRNA regulatory axes such as circRNA_101764/miR-181, circRNA_100338/miR-141-3p, circ-ARL3/miR-1305, circ-ATP5H/miR-138-5p, and several circulating circRNAs were reported to be associated with HBV-HCC development. Notably, TGF/SMAD, JAK/STAT, Notch and Wnt/β-catenin signaling pathways may play pivotal roles in this HBV-driven HCC via several circRNAs. Moreover, in non-HBV HCC patients or HCC patients partially infected by HBV, numerous circRNAs have been identified to be important regulators impacting the malignant biological behavior of HCC. Furthermore, the role of circRNAs in HCC drug resistance has become a focus of research with the aim of reversing chemoresistance and immune resistance. Herein, we review the molecular biology of circRNAs in HBV-HCC and their potential in therapeutic strategies.
Highlights
Hepatocellular carcinoma (HCC), mainly induced by hepatitis B (HBV) or C viral (HCV) infection and accounting for the bulk of primary liver cancers, ranks as the fourth most common cause of cancer-related death globally in 2018 and has a notably poor prognosis [1]
Dozens of circRNAs have been reported to play important biological roles in the occurrence and pathogenesis of HCC progression [5], and they are closely related to immune responses against hepatitis B virus (HBV) infection and regulation of HCC tumorigenesis, including self-sustenance in growth signals, cell proliferation, angiogenesis, cell apoptosis, and tumor metastasis
This study found that metastasis suppressor 1 (MTSS1) is very likely a potential target of miR-141-3p, which may act as an oncogene and a driver of metastasis in HBVassociated HCC (HBV-HCC) through a potential circRNA_100338-miR141-3p-MTSS1 interaction pathway
Summary
Hepatocellular carcinoma (HCC), mainly induced by hepatitis B (HBV) or C viral (HCV) infection and accounting for the bulk of primary liver cancers, ranks as the fourth most common cause of cancer-related death globally in 2018 and has a notably poor prognosis [1]. CircRNAs in HBV-HCC can partially improve the outcomes of these patients, the long-term outcomes are still generally poor [2, 3]. Exploring the molecular biology of valuable biomarkers for early diagnosis of HCC and therapeutic strategies against HCC is extremely important. Many studies have indicated that host circRNAs are involved in immune responses against HBV infection. Dozens of circRNAs have been reported to play important biological roles in the occurrence and pathogenesis of HCC progression [5], and they are closely related to immune responses against HBV infection and regulation of HCC tumorigenesis, including self-sustenance in growth signals, cell proliferation, angiogenesis, cell apoptosis, and tumor metastasis. We discuss the molecular biology underlying HBV-associated HCC (HBVHCC) and thereby provide insight into the role of circRNAs in therapeutic strategies
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