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Featured researches published by Chaohui Zuo.


Proceedings of the National Academy of Sciences of the United States of America | 2014

Complete replication of hepatitis B virus and hepatitis C virus in a newly developed hepatoma cell line

Darong Yang; Chaohui Zuo; Xiaohong Wang; Xianghe Meng; Binbin Xue; Nianli Liu; Rong Yu; Yuwen Qin; Yimin Gao; Qiuping Wang; Jun Hu; Ling Wang; Zebin Zhou; Bing Liu; Deming Tan; Yang Guan; Haizhen Zhu

Significance More than 500 million people are persistently infected with hepatitis B virus (HBV) and/or hepatitis C virus (HCV) and are at a risk of developing chronic hepatitis, cirrhosis, and liver cancer. The absence of robust cell culture systems for both viral infections limits the understanding of the virus lifecycle and pathogenesis required for the development of vaccine and antivirals. We have established a novel human hepatoma cell line termed “HLCZ01” that supports the entire lifecycle of both HBV and HCV produced both in cell culture and clinically. This cell line provides a powerful tool for addressing the virus lifecycle and the development of antivirals and vaccines. The absence of a robust cell culture system for hepatitis B virus (HBV) and hepatitis C virus (HCV) infection has limited the analysis of the virus lifecycle and drug discovery. We have established a hepatoma cell line, HLCZ01, the first cell line, to the authors’ knowledge, supporting the entire lifecycle of both HBV and HCV. HBV surface antigen (HBsAg)-positive particles can be observed in the supernatant and the lumen of the endoplasmic reticulum of the cells via electron microscopy. Interestingly, HBV and HCV clinical isolates propagate in HLCZ01 cells. Both viruses replicate in the cells without evidence of overt interference. HBV and HCV entry are blocked by antibodies against HBsAg and human CD81, respectively, and the replication of HBV and HCV is inhibited by antivirals. HLCZ01 cells mount an innate immune response to virus infection. The cell line provides a powerful tool for exploring the mechanisms of virus entry and replication and the interaction between host and virus, facilitating the development of novel antiviral agents and vaccines.


PLOS ONE | 2011

Innate host response in primary human hepatocytes with hepatitis C virus infection.

Darong Yang; Nianli Liu; Chaohui Zuo; Shoahua Lei; Xinjiao Wu; Fei Zhou; Chen Liu; Haizhen Zhu

Background and Aim The interaction between hepatitis C virus (HCV) and innate antiviral defense systems in primary human hepatocytes is not well understood. The objective of this study is to examine how primary human hepatocytes response to HCV infection. Methods An infectious HCV isolate JFH1 was used to infect isolated primary human hepatocytes. HCV RNA or NS5A protein in the cells was detected by real-time PCR or immunofluorescence staining respectively. Apoptosis was examined with flow cytometry. Mechanisms of HCV-induced IFN-β expression and apoptosis were determined. Results Primary human hepatocytes were susceptible to JFH1 virus and released infectious virus. IFN-α inhibited viral RNA replication in the cells. IFN-β and interferon-stimulated genes were induced in the cells during acute infection. HCV infection induced apoptosis of primary human hepatocytes through the TRAIL-mediated pathway. Silencing RIG-I expression in primary human hepatocytes inhibited IFN-β and TRAIL expression and blocked apoptosis of the cells, which facilitated viral RNA replication in the cells. Moreover, HCV NS34A protein inhibited viral induced IFN-β expression in primary human hepatocytes. Conclusion Innate host response is intact in HCV-infected primary human hepatocytes. RIG-I plays a key role in the induction of IFN and TRAIL by viruses and apoptosis of primary human hepatocytes via activation of the TRAIL-mediated pathway. HCV NS34A protein appears to be capable of disrupting the innate antiviral host responses in primary human hepatocytes. Our study provides a novel mechanism by which primary human hepatocytes respond to natural HCV infection.


Oncology Letters | 2015

Role of antiviral therapy in reducing recurrence and improving survival in hepatitis B virus-associated hepatocellular carcinoma following curative resection (Review)

Chaohui Zuo; Man Xia; Qunfeng Wu; Haizhen Zhu; Jingshi Liu; Chen Liu

Hepatocellular carcinoma (HCC) is one of the major causes of cancer-related mortality worldwide, with the majority of cases associated with persistent hepatitis B virus (HBV) or hepatitis C virus infection. In particular, chronic HBV infection is a predominant risk factor for the development of HCC in Asian and African populations. Hepatic resection, liver transplantion and radiofrequency ablation are increasingly used for the curative treatment of HCC, however, the survival rate of HCC patients who have undergone curative resection remains unsatisfactory due to the high recurrence rate. HCC is a complex disease that is typically resistant to the most commonly used types of chemotherapy and radiotherapy; therefore, the development of novel treatment strategies is required to improve the survival rate of this disease. A high viral load of HBV DNA is the most important correctable risk factor for HCC recurrence, for example nucleos(t)ide analogs improve the outcome following curative resection of HBV-associated HCC, and interferon-α exhibits antitumor activity against various types of cancer via direct inhibitory effects on tumor cells, anti-angiogenesis, enhanced immunogenicity of tumors, immunomodulatory effects and liver dysfunction. In the present review, antiviral treatment for HBV-associated HCC is described as a strategy to reduce recurrence and improve survival.


Oncotarget | 2016

ISG15 in the tumorigenesis and treatment of cancer: An emerging role in malignancies of the digestive system

Chaohui Zuo; Xinyi Sheng; Min Ma; Man Xia; Linda Ouyang

The interferon-stimulated gene 15 ubiquitin-like modifier (ISG15) encodes an IFN-inducible, ubiquitin-like protein. The ISG15 protein forms conjugates with numerous cellular proteins that are involved in a multitude of cellular functions, including interferon-induced immune responses and the regulation of cellular protein turnover. The expression of ISG15 and ISG15-mediated conjugation has been implicated in a wide range of human tumors and cancer cell lines, but the roles of ISG15 in tumorigenesis and responses to anticancer treatments remain largely unknown. In this review, we discuss the findings of recent studies with regard to the role of ISG15 pathways in cancers of the digestive system.


OncoTargets and Therapy | 2017

miRNA-221 of exosomes originating from bone marrow mesenchymal stem cells promotes oncogenic activity in gastric cancer

Min Ma; Shilin Chen; Zhuo Liu; Hailong Xie; Hongyu Deng; Song Shang; Xiaohong Wang; Man Xia; Chaohui Zuo

Worldwide, gastric cancer (GC) is one of the deadliest malignant tumors of the digestive system. Moreover, microRNAs (miRNAs) of exosomes harbored within cancer cells have been determined to induce inflammatory conditions that accelerate tumor growth and metastasis. Interestingly, the oncogenic role of bone marrow mesenchymal stem cells (BM-MSCs) in the modulation of immunosuppression, tumor invasion, and metastasis was discovered to be partly mediated through the secretion of exosomes. In this article, high expression of miRNA-221 (miR-221) in exosomes of the peripheral blood was determined to be positively correlated with the poor clinical prognosis of GC, especially with respect to tumor, node, and metastases stage. Therefore, the expression of miR-221 in exosomes of the peripheral blood may be an important detection index for GC. Proliferation, migration, invasion, and adhesion to the matrix of GC BGC-823 and SGC-7901 cells were significantly enhanced by exosomes that originated from BM-MSCs that were transfected with miR-221 mimics. In conclusion, extracted exosomes from BM-MSCs transfected with miR-221 oligonucleotides can act as high-efficiency nanocarriers, which can provide sufficient miR-221 oligonucleotides to influence the tumor microenvironment and tumor aggressiveness effectively. Notably, the use of a miR-221 inhibitor with an excellent restraining effect in exosomes provides therapeutic potential for GC in future clinical medicine.


Molecular Medicine Reports | 2016

Isolation and comparison of mesenchymal stem cell‑like cells derived from human gastric cancer tissues and corresponding ovarian metastases

Kunyan Zhou; Man Xia; Bo Tang; Darong Yang; Nianli Liu; Dihong Tang; Hailong Xie; Xiaohong Wang; Haizhen Zhu; Chen Liu; Chaohui Zuo

Mesenchymal stem cell (MSC)-like cells have been isolated from various types of tumor. It has previously been reported that MSCs are involved in tumorigenesis and its prognosis. The aim of the present study was to isolate and compare MSC-like cells from human gastric cancer (GC) and its metastatic deposits in ovarian tissue. MSC-like cells were isolated from human gastric cancer (hGC-MSCs) and the corresponding ovarian metastatic tissues (hGCOM-MSCs) from 40 patients. The characteristics of hGC-MSCs and hGCOM-MSCs, including their morphology, surface antigens, specific gene expression and differentiation potential, were similar to those of MSCs derived from human bone marrow (hBM-MSCs) but different from GC cells. In conclusion, the present study demonstrated that MSC-like cells could be isolated from GC tissue and its ovarian metastatic tissues. The existence of MSC-like cells in GC tissues and its ovarian metastatic tissues suggests that they may be a potential target for cancer therapy, and provides an experimental foundation for investigating their role in the initiation and progression of ovarian metastasis of GC.


Cancer Medicine | 2018

MiRNA-545 negatively regulates the oncogenic activity of EMS1 in gastric cancer

Min Ma; Juanxia Zhao; Qunfeng Wu; Ke Xiao; Shuang Li; Haizhen Zhu; Chen Liu; Hailong Xie; Chaohui Zuo

Gastric cancer (GC) is a common malignant tumor of the digestive system. In addition, GC metastasis is an extremely complicated process. In this article, high expression levels of EMS1 mRNA and protein were found to be positively correlated with an enhanced malignant potential of GC cells and a poor clinical prognosis of GC patients. Interestingly, the expression levels of EMS1 mRNA and protein in GC cells were inhibited by microRNA‐545 (miR‐545), which was identified by a bioinformatics analysis. The expression level of miR‐545 in carcinoma tissues was significantly lower than that in para‐carcinoma tissues. The proliferation and epithelial‐mesenchymal transition (EMT) of GC cells were suppressed by exogenous oligonucleotides of miR‐545 mimics. In addition, the expression levels of EMT‐associated markers were altered with the expression of miR‐545. Notably, the growth rates of tumors in nude mice were seriously restrained by an intratumoral injection of oligonucleotides of the miR‐545 mimics. These results suggest a negative regulatory role of miR‐545 on the oncogenic activity of EMS1. In addition, EMS1 and miR‐545 may be potential biomarkers for GC diagnosis. Synthesized oligonucleotides of miR‐545 mimics may be developed as important gene medicines for GC therapy in the future.


Scientific Reports | 2017

Incomplete resection and linitis plastica are factors for poor survival after extended multiorgan resection in gastric cancer patients

Hua Xiao; Min Ma; Yanping Xiao; Yongzhong Ouyang; Ming Tang; Kunyan Zhou; Yuan Hong; Bo Tang; Chaohui Zuo

The aim of this retrospective study was to analyze the morbidity, mortality, and survival rates of extended multiorgan resection (EMR) for locally advanced gastric cancer patients compared to gastrectomy alone and a palliative operation. 893 locally advanced gastric cancer patients without distant metastasis had surgery including gastrectomy alone (GA group, n = 798), EMR resection (EMR group, n = 75), and palliative operation (palliative gastrectomy or gastrojejunostomy (PO group, n = 20)). Postoperative mortality and complication rates in the EMR group were significantly higher than in the GA group (2.7% vs 0.4%, P = 0.010 and 25.3% vs 8.1%, P < 0.001, respectively), but similar in the PO group. The median survival time of the EMR group was significantly longer than in the PO group (27 months vs 11 months, P = 0.020), but significantly worse (P = 0.020) than in the GA group (44 months). Incompleteness of resection (R1) and linitis plastica were independent prognostic factors for survival in the EMR group. Three different gastric cancer surgeries led to different postoperative mortality and complication rates. EMR had a better survival rate compared with PO while GA had the longest survival time with the lowest mortality and complication rates.


Tumor Biology | 2017

MicroRNA-138 enhances TRAIL-induced apoptosis through interferon-stimulated gene 15 downregulation in hepatocellular carcinoma cells

Chaohui Zuo; Xinyi Sheng; Zhuo Liu; Min Ma; Shuhan Xiong; Hongyu Deng; Sha Li; Darong Yang; Xiaohong Wang; Hua Xiao; Hu Quan; Man Xia

Hepatocellular carcinoma is a leading cause of cancer-related mortality worldwide. TRAIL (tumor necrosis factor–related apoptosis–inducing ligand) is a potential target for cancer therapy. However, many cancer cells are resistant to TRAIL-induced apoptosis and its mechanism is not well understood. In this study, to identify potential therapeutic targets for TRAIL-resistant cancer cells, we compared the expression levels of interferon-stimulated gene 15 in TRAIL-sensitive and TRAIL-resistant hepatocellular carcinoma cell lines. Western blot analysis showed that interferon-stimulated gene 15 expression levels were significantly higher in resistant HLCZ01and Huh7 cells than in sensitive LH86 and SMMC-7721 cells. Interferon-stimulated gene 15 knockdown in resistance cells led to TRAIL sensitivity. Conversely, interferon-stimulated gene 15 overexpression in sensitive cells resulted in TRAIL resistance. Our bioinformatics search detected a putative target sequence for microRNA miR-138 in the 3′ untranslated region of the interferon-stimulated gene 15. Real-time quantitative polymerase chain reaction analysis demonstrated that miR-138 was significantly downregulated in TRAIL-resistant cells compared to TRAIL-sensitive cells. Forced expression of miR-138 in resistant cells decreased both messenger RNA and protein levels of interferon-stimulated gene 15, and when exposed to TRAIL, activated poly(adenosine diphosphate-ribose) polymerase, indicating sensitization to TRAIL. The results suggested that miR-138 regulates the interferon-stimulated gene 15 expression by directly targeting the 3′ untranslated region of interferon-stimulated gene 15 and modulates the sensitivity to TRAIL-induced apoptosis. MiR-138 may be a target for therapeutic intervention in TRAIL-based drug treatments of resistant hepatocellular carcinoma or could be a biomarker to select patients who may benefit from the treatment.


Oncotarget | 2014

miR-942 decreases TRAIL-induced apoptosis through ISG12a downregulation and is regulated by AKT

Nianli Liu; Chaohui Zuo; Xiaohong Wang; Tianran Chen; Darong Yang; Jing Wang; Haizhen Zhu

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Min Ma

Central South University

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Hua Xiao

Central South University

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Man Xia

Central South University

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Zhuo Liu

Central South University

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Bo Tang

Central South University

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