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213 results on '"Andrisani, Ourania"'

3. A roadmap for serum biomarkers for hepatitis B virus: current status and future outlook

Author

Kramvis, Anna, Chang, Kyong-Mi, Dandri, Maura, Farci, Patrizia, Glebe, Dieter, Hu, Jianming, Janssen, Harry L. A., Lau, Daryl T. Y., Penicaud, Capucine, Pollicino, Teresa, Testoni, Barbara, Van Bömmel, Florian, Andrisani, Ourania, Beumont-Mauviel, Maria, Block, Timothy M., Chan, Henry L. Y., Cloherty, Gavin A., Delaney, William E., Geretti, Anna Maria, Gehring, Adam, Jackson, Kathy, Lenz, Oliver, Maini, Mala K., Miller, Veronica, Protzer, Ulrike, Yang, Jenny C., Yuen, Man-Fung, Zoulim, Fabien, and Revill, Peter A.

Published
2022
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21. RNA helicase DDX5 enables STAT1 mRNA translation and interferon signalling in hepatitis B virus replicating hepatocytes

Author

Sun, Jiazeng, primary, Wu, Guanhui, additional, Pastor, Florentin, additional, Rahman, Naimur, additional, Wang, Wen-Hung, additional, Zhang, Zhengtao, additional, MERLE, Philippe, additional, Hui, Lijian, additional, Salvetti, Anna, additional, Durantel, David, additional, Yang, Danzhou, additional, and Andrisani, Ourania, additional

Published
2021
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30. Restoration of RNA helicase DDX5 suppresses hepatitis B virus (HBV) biosynthesis and Wnt signaling in HBV-related hepatocellular carcinoma

Author

Mani, Saravana Kumar Kailasam, primary, Yan, Bingyu, additional, Cui, Zhibin, additional, Sun, Jiazeng, additional, Utturkar, Sagar, additional, Foca, Adrien, additional, Fares, Nadim, additional, Durantel, David, additional, Lanman, Nadia, additional, Merle, Philippe, additional, Kazemian, Majid, additional, and Andrisani, Ourania, additional

Published
2020
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33. RNA Helicase DDX5 Negatively Regulates Wnt Signaling and Hepatocyte Reprogramming in Hepatitis B Virus-related Hepatocellular Carcinoma

Author

Mani, Saravana Kumar Kailasam, Cui, Zhibin, Yan, Bingyu, Utturkar, Sagar, Foca, Adrien, Fares, Nadim, Durantel, David, Lanman, Nadia, Merle, Philippe, Kazemian, Majid, and Andrisani, Ourania

Subjects
Hepatitis B virus, 0303 health sciences, Gene knockdown, DDX5, Wnt signaling pathway, Biology, HCCS, medicine.disease_cause, RNA Helicase A, digestive system diseases, 3. Good health, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Viral replication, chemistry, 030220 oncology & carcinogenesis, microRNA, medicine, Cancer research, 030304 developmental biology
Abstract

Background and AimsRNA helicase DEAD box protein 5 (DDX5) is downregulated during hepatitis B virus (HBV) replication, and associates with poor prognosis HBV-related hepatocellular carcinoma (HCC). The aim of this study is to determine the mechanism and significance of DDX5 downregulation for HBV-driven HCC.Approach & ResultsWe used established cellular models of HBV replication, HBV infection, as well as HBV-related liver tumors. HBV replicating DDX5 knockdown hepatocytes were analyzed by RNAseq; differentially expressed genes were validated by qRT-PCR, and bioinformatic analyses of HCCs from The Cancer Genome Atlas. Our results show reduced expression of DDX5 in HCCs of all etiologies is associated with poor survival. In HBV replicating hepatocytes, downregulation of DDX5 is mediated by miR17∼92 and miR106b∼25, induced by HBV infection. Increased expression of these miRNAs was quantified in HBV-associated HCCs expressing a hepatic cancer stem cell (hCSC)-like gene signature and reduced DDX5 mRNA, suggesting a role for DDX5 in hCSC formation. Interestingly, DDX5 knockdown in HBV replicating hepatocyte cell lines resulted in hepatosphere formation, sorafenib and cisplatin resistance, Wnt signaling activation and pluripotency gene expression, all characteristics of hCSCs. Moreover, DDX5 knockdown increased viral replication. RNA-seq analyses of HBV-replicating DDX5 knockdown cells, identified enhanced expression of key genes of the Wnt/β-catenin pathway, including Frizzled7 (FZD7) and Matrix Metallopeptidase7 (MMP7), indicative of Wnt signaling activation. Clinically, elevated FZD7 expression correlates with poor patient survival. Importantly, inhibitors to miR17∼92 and miR106b∼25 restored DDX5 levels and suppressed both Wnt/β-catenin activation and viral replication.ConclusionDDX5 is a negative regulator of Wnt signaling and hepatocyte reprogramming in HCCs. Restoration of DDX5 levels in HBV-infected patients can exert both antitumor and antiviral effects.

Published
2019

37. Inhibition of interferon signaling during Hepatitis B Virus infection and virus-associated hepatocellular carcinoma

Author

Mani, Saravana Kumar Kailasam and Andrisani, Ourania

Subjects
Hepatitis B virus, Carcinoma, Hepatocellular, Liver Neoplasms, Hepatitis B, digestive system diseases, Article, Immunity, Innate, Hepatitis B, Chronic, STAT1 Transcription Factor, Neoplastic Stem Cells, Animals, Humans, Interferons, Signal Transduction
Abstract

Chronic Hepatitis B Virus (HBV) infection is linked to hepatocellular carcinoma (HCC) pathogenesis. The World Health Organization estimates that globally 257 million people are chronic HBV carriers at risk of developing liver cancer. Current therapies for prevention and treatment of HCC are inadequate. Although interferon-based treatment strategies hold great promise for combating chronic infection and HCC, many patients do not respond to the IFN-based drugs for reasons not completely understood. Interferon signaling plays key roles in activation of innate and adaptive immunity. However, HBV has evolved various mechanisms to suppress IFN signaling. In this review, we present the basics about HBV infection and interferon signaling. Next, we discuss mechanisms through which HBV downregulates the function -activity and transcription- of the transcription factor STAT1 during acute and chronic infection. STAT1 is activated in response to all types (I/II/III) of interferon signaling and is essential in mediating all types (I/II/III) of interferon responses. Lastly, we discuss emerging evidence from different human cancers linking loss of interferon signaling to aggressive cancer and cancer stem cells. Whether the same occurs during HBV-associated hepatocarcinogenesis is discussed and currently under investigation.

Published
2018

38. RNA Helicase DDX5 Negatively Regulates Wnt Signaling and Hepatocyte Reprogramming in Hepatitis B Virus-related Hepatocellular Carcinoma

Author

Mani, Saravana Kumar Kailasam, primary, Cui, Zhibin, additional, Yan, Bingyu, additional, Utturkar, Sagar, additional, Foca, Adrien, additional, Fares, Nadim, additional, Durantel, David, additional, Lanman, Nadia, additional, Merle, Philippe, additional, Kazemian, Majid, additional, and Andrisani, Ourania, additional

Published
2019
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40. RNA helicase DDX5 enables STAT1 mRNA translation and interferon signalling in hepatitis B virus replicating hepatocytes

Author

Sun, Jiazeng, Wu, Guanhui, Pastor, Florentin, Rahman, Naimur, Wang, Wen-Hung, Zhang, Zhengtao, MERLE, Philippe, Hui, Lijian, Salvetti, Anna, Durantel, David, Yang, Danzhou, and Andrisani, Ourania

Abstract

ObjectiveRNA helicase DDX5 is downregulated during HBV replication and poor prognosis HBV-related hepatocellular carcinoma (HCC). The objective of this study is to investigate the role of DDX5 in interferon (IFN) signalling. We provide evidence of a novel mechanism involving DDX5 that enables translation of transcription factor STAT1 mediating the IFN response.Design and resultsMolecular, pharmacological and biophysical assays were used together with cellular models of HBV replication, HCC cell lines and liver tumours. We demonstrate that DDX5 regulates STAT1 mRNA translation by resolving a G-quadruplex (rG4) RNA structure, proximal to the 5′ end of STAT1 5′UTR. We employed luciferase reporter assays comparing wild type (WT) versus mutant rG4 sequence, rG4-stabilising compounds, CRISPR/Cas9 editing of the STAT1-rG4 sequence and circular dichroism determination of the rG4 structure. STAT1-rG4 edited cell lines were resistant to the effect of rG4-stabilising compounds in response to IFN-α, while HCC cell lines expressing low DDX5 exhibited reduced IFN response. Ribonucleoprotein and electrophoretic mobility assays demonstrated direct and selective binding of RNA helicase-active DDX5 to the WT STAT1-rG4 sequence. Immunohistochemistry of normal liver and liver tumours demonstrated that absence of DDX5 corresponded to absence of STAT1. Significantly, knockdown of DDX5 in HBV infected HepaRG cells reduced the anti-viral effect of IFN-α.ConclusionRNA helicase DDX5 resolves a G-quadruplex structure in 5′UTR of STAT1 mRNA, enabling STAT1 translation. We propose that DDX5 is a key regulator of the dynamic range of IFN response during innate immunity and adjuvant IFN-α therapy.

Published
2022
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46. Notch activation drives adipocyte dedifferentiation and tumorigenic transformation in mice

Author

Bi, Pengpeng, primary, Yue, Feng, additional, Karki, Anju, additional, Castro, Beatriz, additional, Wirbisky, Sara E., additional, Wang, Chao, additional, Durkes, Abigail, additional, Elzey, Bennett D., additional, Andrisani, Ourania M., additional, Bidwell, Christopher A., additional, Freeman, Jennifer L., additional, Konieczny, Stephen F., additional, and Kuang, Shihuan, additional

Published
2016
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47. RNA helicase DEAD box protein 5 regulates Polycomb repressive complex 2/Hox transcript antisense intergenic RNA function in hepatitis B virus infection and hepatocarcinogenesis

Author

Zhang, Hao, primary, Xing, Zheng, additional, Mani, Saravana Kumar Kailasam, additional, Bancel, Brigitte, additional, Durantel, David, additional, Zoulim, Fabien, additional, Tran, Elizabeth J., additional, Merle, Philippe, additional, and Andrisani, Ourania, additional

Published
2016
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48. Stilbenoids remodel the DNA methylation patterns in breast cancer cells and inhibit oncogenic NOTCH signaling through epigenetic regulation of MAML2 transcriptional activity

Author

Lubecka, Katarzyna, primary, Kurzava, Lucinda, additional, Flower, Kirsty, additional, Buvala, Hannah, additional, Zhang, Hao, additional, Teegarden, Dorothy, additional, Camarillo, Ignacio, additional, Suderman, Matthew, additional, Kuang, Shihuan, additional, Andrisani, Ourania, additional, Flanagan, James M., additional, and Stefanska, Barbara, additional

Published
2016
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50. Comparative study of visible light polymerized gelatin hydrogels for 3D culture of hepatic progenitor cells.

Author

Greene, Tanja, Lin, Tsai‐Yu, Andrisani, Ourania M., and Lin, Chien‐Chi

Subjects
PHOTOPOLYMERIZATION kinetics, ELECTROMAGNETIC waves, ELECTROMAGNETIC wave propagation, HYDROGELS, EXPANSION microscopy
Abstract

ABSTRACT Photopolymerization techniques have been widely used to create hydrogels for biomedical applications. Visible light-based photopolymerizations are commonly initiated by type II (i.e., noncleavage-type) photoinitiator in conjunction with a coinitiator. On the other hand, type I photoinitiators (i.e., cleavage type) are rarely compatible with visible light-based initiation due to their limited molar absorbability in the visible light wavelengths. Here, we report visible light initiated orthogonal photoclick crosslinking to fabricate gelatin-norbornene and poly(ethylene glycol)-tetra-thiol hydrogels using either cleavage-type (i.e., lithium acylphosphinate, LAP) or noncleavage-type photoinitiator (i.e., eosin-Y, EY) without the use of a coinitiator. Regardless of the initiator type, the step-growth gelatin-PEG hybrid hydrogels crosslinked and degraded similarly. While both systems exhibited similar cytocompatibility for hepatic progenitor HepaRG cells, gelation initiated by noncleavage-type initiator EY afforded slightly higher degree of hepatic gene expression. © 2016 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2017, 134, 44585. [ABSTRACT FROM AUTHOR]

Published
2017
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