Functional sequestration of microRNA-122 from Hepatitis C Virus by circular RNA sponges

Jost, Isabelle; Shalamova, Lyudmila; Gerresheim, Gesche K.; Niepmann, Michael; Bindereif, Albrecht; Roßbach, Oliver

doi:10.1080/15476286.2018.1435248

Cited by 107 publications

(155 citation statements)

References 41 publications

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“…Several clinical studies have demonstrated that the inhibitors of miR‐122 play an important role in reducing viral load in HCV patients with chronic infection. Other researchers have designed circRNA sponges to absorb miR‐122 . Such artificial circRNAs possess the capacity to mount inhibition on viral protein synthesis, hence leading to the suppression of HCV replication.…”

Section: Circrnas Block the Hepatitis Virus Infectionmentioning

confidence: 99%

Molecular mechanisms of circular RNAs, transforming growth factor‐β, and long noncoding RNAs in hepatocellular carcinoma

Shang

Adzika

et al. 2019

Cancer Medicine

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At the heart of hepatocellular carcinoma (HCC) lies disruption of signaling pathways at the level of molecules, genes, and cells. Non‐coding RNAs (ncRNAs) have been implicated in the disease progression of HCC. For instance, dysregulated expression of circular RNAs (circRNAs) has been observed in patients with HCC. As such, these RNAs are potential therapeutic targets and diagnostic markers for HCC. Long non‐coding RNAs (lncRNAs), a type of ncRNA, have also been recognized to participate in the initiation and progression of HCC. Transforming growth factor‐beta (TGF‐β) is another element which is now recognized to play crucial roles in HCC. It has been implicated in many biological processes such as survival, immune surveillance, and cell proliferation. In HCC, TGF‐β promotes disease progression by two mechanisms: an intrinsic signaling pathway and the extrinsic pathway. Through these pathways, it modulates various microenvironment factors such as inflammatory mediators and fibroblasts. An interesting yet‐to‐be resolved concept is whether the HCC‐promoting role of TGF‐β pathways is limited to a subset of HCC patients or it is involved in the whole process of HCC development. This review summarizes recent advancements to highlight the roles of circRNAs, lncRNAs, and TGF‐β in HCC.

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Section: Circrnas Block the Hepatitis Virus Infectionmentioning

confidence: 99%

Molecular mechanisms of circular RNAs, transforming growth factor‐β, and long noncoding RNAs in hepatocellular carcinoma

Shang

Adzika

et al. 2019

Cancer Medicine

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“…Many viruses, including KSHV, encode miRNAs and target human or viral transcripts (12). Recently, miR-122 targeting artificial circRNAs was designed and proven to have antiviral capacity (13). These developments raise the possibility that natural human circular RNAs can potentially act as antiviral molecules if they contain binding sites for…”

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confidence: 99%

Discovery of Kaposi’s sarcoma herpesvirus-encoded circular RNAs and a human antiviral circular RNA

Tagawa

Gao

Kopardé

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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186

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Noncoding RNAs have substantial effects in host–virus interactions. Circular RNAs (circRNAs) are novel single-stranded noncoding RNAs which can decoy other RNAs or RNA-binding proteins to inhibit their functions. The role of circRNAs is largely unknown in the context of Kaposi’s sarcoma herpesvirus (KSHV). We hypothesized that circRNAs influence viral infection by inhibiting host and/or viral factors. Transcriptome analysis of KSHV-infected primary endothelial cells and a B cell line identified human circRNAs that are differentially regulated upon infection. We confirmed the expression changes with divergent PCR primers and RNase R treatment of specific circRNAs. Ectopic expression of hsa_circ_0001400, a circRNA induced by infection, suppressed expression of key viral latent gene LANA and lytic gene RTA in KSHV de novo infections. Since human herpesviruses express noncoding RNAs like microRNAs, we searched for viral circRNAs encoded in the KSHV genome. We performed circRNA-Seq analysis with RNase R-treated, circRNA-enriched RNA from KSHV-infected cells. We identified multiple circRNAs encoded by the KSHV genome that are expressed in KSHV-infected endothelial cells and primary effusion lymphoma (PEL) cells. The KSHV circRNAs are located within ORFs of viral lytic genes, are up-regulated upon the induction of the lytic cycle, and alter cell growth. Viral circRNAs were also detected in lymph nodes from patients of KSHV-driven diseases such as PEL, Kaposi’s sarcoma, and multicentric Castleman’s disease. We revealed new host–virus interactions of circRNAs: human antiviral circRNAs are activated in response to KSHV infection, and viral circRNA expression is induced in the lytic phase of infection.

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“…8 Generally, 5-FU is commonly used to treat BC. [10][11][12] CircRNAs are proved as potential biomarkers in many diseases including hepatoma carcinoma and other cancers. 9 Circular RNA (CircRNA) is a naturally occurring family of noncoding RNAs, which has been commonly detected in viruses, plant and animals.…”

Section: -Fluorouracil (5-fu) Is Well-known For Its Anti-tumour Effectmentioning

confidence: 99%

“…9 Circular RNA (CircRNA) is a naturally occurring family of noncoding RNAs, which has been commonly detected in viruses, plant and animals. [10][11][12] CircRNAs are proved as potential biomarkers in many diseases including hepatoma carcinoma and other cancers. 13 CDR1as (also known as CiRS-7), one of the thousands of CircRNAs, was recently demonstrated to function as a powerful miR-7 sponge/ inhibitor in developing midbrain of zebrafish, suggesting a novel mechanism for regulating microRNA functions.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of circular RNA CDR1as increases chemosensitivity of 5‐FU‐resistant BC cells through up‐regulating miR‐7

Yang

Wang

et al. 2019

J Cellular Molecular Medi

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This study aims to explore the mechanism of Circular RNA CDR1as implicating in regulating 5‐fluorouracil (5‐FU) chemosensitivity in breast cancer (BC) by competitively inhibiting miR‐7 to regulate CCNE1. Expressions of CDR1as and miR‐7 in 5‐FU‐resistant BC cells were determined by RT‐PCR. CCK‐8, colony formation assay and flow cytometry were applied to measure half maximal inhibitory concentration (IC50), 5‐Fu chemosensitivity and cell apoptosis. Western blot was used to detect the expressions of apoptosis‐related factors. CDR1as was elevated while miR‐7 was inhibited in 5‐FU‐resistant BC cells. Cells transfected with si‐CDR1as or miR‐7 mimic had decreased IC50 and colony formation rate, increased expressions of Bax/Bcl2 and cleaved‐Caspase‐3/Caspase‐3, indicating inhibition of CDR1as and overexpression of miR‐7 enhances the chemosensitity of 5‐FU‐resistant BC cells. Targetscan software indicates a binding site of CDR1as and miR‐7 and that CCNE1 is a target gene of miR‐7. miR‐7 can gather CDR1as in BC cells and can inhibit CCNE1. In comparison to si‐CDR1as group, CCNE1 was increased and chemosensitivity to 5‐Fu was suppressed in si‐CDR1as + miR‐7 inhibitor group. When compared with miR‐7 mimic group, CDR1as + miR‐7 mimic group had increased CCNE1 and decreased chemosensitivity to 5‐Fu. Nude mouse model of BC demonstrated that the growth of xenotransplanted tumour in si‐CDR1as + miR‐7 inhibitor group was faster than that in si‐CDR1as group. The tumour growth in CDR1as + miR‐7 mimic group was faster than that in miR‐7 mimic group. CDR1as may regulate chemosensitivity of 5‐FU‐resistant BC cells by inhibiting miR‐7 to regulate CCNE1.

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Functional sequestration of microRNA-122 from Hepatitis C Virus by circular RNA sponges

Cited by 107 publications

References 41 publications

Molecular mechanisms of circular RNAs, transforming growth factor‐β, and long noncoding RNAs in hepatocellular carcinoma

Molecular mechanisms of circular RNAs, transforming growth factor‐β, and long noncoding RNAs in hepatocellular carcinoma

Discovery of Kaposi’s sarcoma herpesvirus-encoded circular RNAs and a human antiviral circular RNA

Inhibition of circular RNA CDR1as increases chemosensitivity of 5‐FU‐resistant BC cells through up‐regulating miR‐7

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