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6 results on '"Yan, Bingyu"'

1. A comprehensive single cell data analysis of in lymphoblastoid cells reveals the role of Super-enhancers in maintaining EBV latency

Author

Yan, Bingyu, primary, Wang, Chong, additional, Chakravorty, Srishti, additional, Zhang, Zonghao, additional, Kadadi, Simran D., additional, Zhuang, Yuxin, additional, Sirit, Isabella, additional, Hu, Yonghua, additional, Jung, Minwoo, additional, Sahoo, Subhransu, additional, Wang, Luopin, additional, Shao, Kunming, additional, Anderson, Nicole L., additional, Trujillo-Ochoa, Jorge L., additional, Liu, Xing, additional, Olson, Matthew R., additional, Afzali, Behdad, additional, Zhao, Bo, additional, and Kazemian, Majid, additional

Published
2022
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3. Host-virus chimeric events in SARS-CoV2 infected cells are infrequent and artifactual

Author

Yan, Bingyu, primary, Chakravorty, Srishti, additional, Mirabelli, Carmen, additional, Wang, Luopin, additional, Trujillo-Ochoa, Jorge L., additional, Chauss, Daniel, additional, Kumar, Dhaneshwar, additional, Lionakis, Michail S., additional, Olson, Matthew R, additional, Wobus, Christiane E., additional, Afzali, Behdad, additional, and Kazemian, Majid, additional

Published
2021
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4. An autocrine Vitamin D-driven Th1 shutdown program can be exploited for COVID-19

Author

McGregor, Reuben, primary, Chauss, Daniel, additional, Freiwald, Tilo, additional, Yan, Bingyu, additional, Wang, Luopin, additional, Nova-Lamperti, Estefania, additional, Zhang, Zonghao, additional, Teague, Heather, additional, West, Erin E, additional, Bibby, Jack, additional, Kelly, Audrey, additional, Malik, Amna, additional, Freeman, Alexandra F, additional, Schwartz, Daniella, additional, Portilla, Didier, additional, John, Susan, additional, Lavender, Paul, additional, Lionakis, Michail S, additional, Mehta, Nehal N, additional, Kemper, Claudia, additional, Cooper, Nichola, additional, Lombardi, Giovanna, additional, Laurence, Arian, additional, Kazemian, Majid, additional, and Afzali, Behdad, additional

Published
2020
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5. 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

6. 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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