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Oncogenic Wnt3a is a promising sensitive biomarker for monitoring hepatocarcinogenesis

Hepatobiliary & Pancreatic Diseases International 2023年第3期22卷 263-269页

作者： Min Yao Jian-Jun Wang Xi-Yu Chen Wen-Li Sai Jie Yang De-Feng Wang Li Wang Deng-Fu Yao Research Center of Clinical Medicine Affiliated Hospital of Nantong UniversityNantong 226001China Department of Immunology Medical School of Nantong UniversityNantong 226001China Nantong Health College of Jiangsu Province Nantong 226016China Department of Molecular Biology Life Science School of Nantong UniversityNantong 226019China Research Center for Intelligence Information Technology of Nantong University Nantong 226019China

Background:The effective treatment for hepatocellular carcinoma(HCC)depends on early ***,the abnormal expression of Wnt3a as the key signaling molecule in the Wnt/β-catenin pathway was found in HCC cells and could be released into the *** this study,we used rat model of hepatocarcinogenesis to dynamically investigate the alteration of oncogenic Wnt3a and to explore its early monitor value for ***:Sprague-Dawley rats(SD)were fed with diet 2-fluorenylacetamide(2-FAA,0.05%)for inducing hepatocarcinogenesis,and grouped based on liver morphological alteration by Hematoxylin&Eosin(H&E)staining;rats fed with normal chow were used as normal control(NC).Total RNA and protein were purified from rat *** expressed genes(DEGs)or Wnt3a m RNA,cellular distribution,and Wnt3a protein levels were analyzed by whole genome microarray with signal logarithm ratio(SLR log 2 cy5/cy3),immunohistochemistry,and enzyme-linked immunosorbent assay,***:Models of rat hepatocarcinogenesis were successfully established based on liver histopathological H&E *** were divided into the cell degeneration(r Deg),precancerosis(r Pre-C)and HCC(r HCC)*** numbers of the up-and down-regulated DEGs with SLR≥8 were 55 and 48 in the r Deg group,268 and 57 in the r Pre-C group,and 312 and 201 in the r HCC group,*** altered genes were involved in cell proliferation,signal transduction,tumor metastasis,and *** with the NC group,Wnt3a m RNA was increased by 4.6 folds(P<0.001)in the r Deg group,7.4 folds(P<0.001)in the r Pre-C group,and 10.4 folds(P<0.001)in the r HCC group;the positive rates of liver Wnt3a were 66.7%(P=0.001)in the r Deg group,100%(P<0.001)in the r Pre-C group,and 100%(P<0.001)in the r HCC group,***,there were significant differences of liver Wnt3a(P<0.001)or serum Wnt3a(P<0.001)among different ***:Overexpression of Wnt3a was associated with rat hepa

关键词： hepatocarcinogenesis Dynamic expression Monitoring Model

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From liver fibrosis to hepatocarcinogenesis: Role of excessive liver H_(2)O_(2) and targeting nanotherapeutics

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Bioactive Materials 2023年第5期23卷 187-205页

作者： Meiyu Shao Yifan Wang Hongyan Dong Lu Wang Xiaoqing Zhang Xin Han Xianan Sang Yini Bao Mengyun Peng Gang Cao School of Pharmacy Zhejiang Chinese Medical UniversityHangzhou310000PR China

Liver fibrosis and hepatocellular carcinoma(HCC)have been worldwide threats *** fibrosis is reversible in early stages but will develop precancerosis of HCC in cirrhotic *** pathological liver,excessive H_(2)O_(2) is generated and accumulated,which impacts the functionality of hepatocytes,Kupffer cells(KCs)and hepatic stellate cells(HSCs),leading to genesis of fibrosis and HCC.H_(2)O_(2) accumulation is associated with overproduction of superoxide anion(O_(2)^(·-))and abolished antioxidant enzyme *** of therapeutics focused on H_(2)O_(2) have shown satisfactory effects against liver fibrosis or HCC in different *** review summarized the reasons of liver H_(2)O_(2) accumulation,and the role of H_(2)O_(2) in genesis of liver fibrosis and ***,nanotherapeutics targeting H_(2)O_(2) were summarized for further consideration of antifibrotic or antitumor therapy.

关键词： Liver fibrosis hepatocarcinogenesis Nanotherapeutics H_(2)O_(2)accumulation Oxidative stress

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A single dose of caffeic acid phenethyl ester prevents initiation in a medium-term rat hepatocarcinogenesis model

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World Journal of Gastroenterology 2006年第42期12卷 6779-6785页

作者： Claudia Esther Carrasco-Legleu Yesennia Sánchez-Pérez Lucrecia Márquez-Rosado Samia Fattel-Fazenda Evelia Arce-Popoca Sergio Hernández-García Saúl Villa-Trevio Departamento de Biología Celular Centro de Investigación y de Estudios Avanzados del IPN (Cinvestav). Ave. IPN #2508. Col. San Pedro Zacatenco C.P. 07360 México D.F. México Instituto Nacional de Cancerología San Fernando No. 22 C.P.14080 México D.F. México

AIM： To study of the effect of caffeic acid phenethyl ester （CAPE） on the initiation period in a medium-term assay of hepatocarcinogenesis. METHODS： Male Wistar rats were subjected to a carcinogenic treatment （CT） and sacrificed at 25^th d; altered hepatic foci （AHF） were generated efficiently. To a second group of rats a single 20 mg/kg doses of CAPE was given 12 h before initiation with CT and were sacrificed at 25^th d. We evaluated the expression of preneoplastic markers as Y-glutamyltranspeptidase （GGT） and glutathione S-transferase type pi protein （GSTp） by histochemistry, RT-PCR and Western blot analyses, respectively. We measured thiobarbituric acid reactive substances （TBARS） in homogenates of liver and used Unscheduled DNA Synthesis （UDS） assay by incorporation of [^3H] thymidine （^3HdT） in primary hepatocyte cultures （PHC）. RESULTS： At 25^th d after CT CAPE reduced the observed increase of GGT^＋AHF by 84% and liver expression ofggt mRNA by 100%. In case of the GSTp protein, the level was reduced by 90%. As indicative of oxidative stress generated by diethylnitrosamine （DEN） 12 h after its administration, we detected a 68% increase of TBARS. When CAPE was administered before DEN, it completely protected from liver TBARS induction. To have an indication of the sole effect of CAPE on initiation, two carcinogens were tested in a UDS assay in PHC, we used methyl-n-nitrosoguanidine as a direct carcinogen and DEN, as indirect carcinogen. In this assay, genotoxic damage caused by carcinogens was abolished at 5μM CAPE concentration. CONCLUSION： Our results demonstrated that CAPE possesses anti-genotoxic and antineoplastic capabilities, by an anti-oxidative and free-radical scavenging mechanism.

关键词： Caffeic acid phenethyl ester Antioxidant hepatocarcinogenesis Initiation

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Abnormal CD44 activation of hepatocytes with nonalcoholic fatty accumulation in rat hepatocarcinogenesis

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World Journal of Gastrointestinal Oncology 2020年第1期12卷 66-76页

作者： Miao Fang Min Yao Jie Yang Wen-Jie Zheng Li Wang Deng-Fu Yao Medical School of Nantong University Nantong 226001Jiangsu ProvinceChina Research Center of Clinical Medicine Affiliated Hospital of Nantong UniversityNantong 226001Jiangsu ProvinceChina Department of Medical Informatics Medical School of Nantong UniversityNantong 226001Jiangsu ProvinceChina

BACKGROUND Prevalence of nonalcoholic fatty liver disease(NAFLD)is rapidly increasing,and NAFLD has become one of the most common chronic liver diseases *** abnormal CD44 activation,the severe form of NAFLD can progress to liver cirrhosis and hepatocellular carcinoma(HCC).Thus,the molecular mechanism of CD44 in NAFLD needs to be *** To investigate the relationship between CD44 activation and malignant transformation of rat hepatocytes under nonalcoholic lipid *** Sprague-Dawley rats were fed a high-fat(HF)for 12 wk to entice NAFLD and then with HF plus 2-fluorenylacetamide(0.05%)to induce *** were sacrificed every 2 wk,and subsequently divided into the groups based on liver pathological examination(hematoxylin and eosin staining):NAFLD,denaturation,precancerosis,HCC,and *** CD44 mRNA was detected by *** fat as assessed by Oil red O staining or CD44 by immunohistochemical assay was compared with their integral optic *** CD44,alanine aminotransferase,aspartate aminotransferase,triglyceride,total cholesterol,and AFP levels were quantitatively *** Elevated CD44 was first reported in hepatocarcinogenesis,with increasing expression from NAFLD to HCC at the protein or mRNA *** CD44 integral optic density values were significantly different between the control group and the NAFLD(t=25.433,P<0.001),denaturation(t=48.822,P<0.001),precancerosis(t=27.751,P<0.001),and HCC(t=16.239,P<0.001)groups,*** CD44 can be secreted into the blood,and serum CD44 levels in HCC or precancerous rats were significantly higher(P<0.001)than those in any of the other *** correlations were found between liver CD44 and CD44 mRNA(rs=0.373,P=0.043)and serum CD44(rs=0.541,P=0.002)and between liver CD44 mRNA and serum CD44(rs=0.507,P=0.004).Moreover,significant correlations were found between liver CD44 and liver AFP(rs=0.572,P=0.001),between serum CD44 and serum AFP(rs=0.608,P<0.001),an

关键词： hepatocarcinogenesis CD44 Nonalcoholic fatty liver disease Animal model Dynamic expressions

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Role of hepatitis B virus DNA integration in human hepatocarcinogenesis

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World Journal of Gastroenterology 2014年第20期20卷 6236-6243页

作者： Hoang Hai Akihiro Tamori Norifumi Kawada Department of Hepatology Osaka City University Graduate School of Medicine Osaka 5458585 Japan

Liver cancer ranks sixth in cancer incidence, and is the third leading cause of cancer-related deaths worldwide. Hepatocellular carcinoma (HCC) is the most common type of liver cancer, which arises from hepatocytes and accounts for approximately 70%-85% of cases. Hepatitis B virus (HBV) frequently causes liver inflammation, hepatic damage and subsequent cirrhosis. Integrated viral DNA is found in 85%-90% of HBV-related HCCs. Its presence in tumors from non-cirrhotic livers of children or young adults further supports the role of viral DNA integration in hepatocarcinogenesis. Integration of subgenomic HBV DNA fragments into different locations within the host DNA is a significant feature of chronic HBV infection. Integration has two potential consequences: (1) the host genome becomes altered (“cis” effect); and (2) the HBV genome becomes altered (“trans” effect). The cis effect includes insertional mutagenesis, which can potentially disrupt host gene function or alter host gene regulation. Tumor progression is frequently associated with rearrangement and partial gain or loss of both viral and host sequences. However, the role of integrated HBV DNA in hepatocarcinogenesis remains controversial. Modern technology has provided a new paradigm to further our understanding of disease mechanisms. This review summarizes the role of HBV DNA integration in human carcinogenesis.

关键词： Hepatitis B virus Integration hepatocarcinogenesis Cis effect Trans effect Whole genome sequencing

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Glutathione S-Transferase Isoenzymes as Marker in Preneoplasia of Rat Chemical hepatocarcinogenesis

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Chinese Science Bulletin 1993年第7期38卷 602-607页

作者：左瑾方福德丁濂谢大英 Institute of Basic Medical Sciences Chinese Academy of Medical Sciences Beijing 100005 PRC Institute of Occupational Medicine Chinese Academy of Preventive Medicine Beijing 100050 PRC

It has been generally accepted that about 85％ of cancers are caused by chemical factors and the chemically induced carcinogenic process can be divided into two or three stages, i. e. initiation and promotion, or together with further progression. The initiation is usually considered to be an irreversible process, but it can be blocked to further progress to cancer. For this reason, searching of objective markers for identifying initiated cells has played an important role in defining the preneoplastic lesion. So far, a large number of studies have been carried out on this object, including biochemistry, histopathology, histochemistry, immunohistochemistry, etc., and nearly thirty histochemical and other phenotypic changes have been found associated with the putative preneoplastic liver

关键词： GST-isoenzyme chemicai hepatocarcinogenesis isoelectric focusing marker enzyme.

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Lipid metabolic reprogramming promotes hepatocarcinogenesis and targeted regulation of related drugs

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中国药理学与毒理学杂志 2019年第10期 788-789页

作者： ZHANG Cong QIU Zhen-peng ZHENG Guo-hua College of Pharmacy Hubei University of Chinese Medicine Key Laboratory of Chinese Medicine Resource and Compound Prescription Ministry of Education Hubei University of Chinese Medicine

Reprogramming of lipid metabolism is the central link leading to malignant transformation of cells into tumors and metabolic reprogramming fueling cell proliferation and survival is a potential hallmark of tumor initiation and progression. As the central regulating organ of lipid metabolism, the reprogrammed over activation of liver lipid metabolism can lead to malignant transformation of hepatocytes and promote the occurrence of hepatocarcinogenesis. hepatocarcinogenesis attributes to the cumulatively somatic genomic and epigenomic alterations considered "drivers" deregulating multiple signaling pathways. Mounting evidence suggests that, excessive activation of the v-akt murine thymoma viral oncogene homolog（AKT）/mammalian target of rapamycin（m TOR）signal transduction cascades frequently activates the SREBP-1/FASN-mediated de novolipogenic pathway and accelerated hepatocarcinogenesis. Importantly, AKT is the major regulator of FASN-mediated de novo lipogenesis during tumor development and progression. OBJECTIVE To study the effect of FASN inhibitor orlistat on targeting lipid metabolism reprogramming in hepatocellular carcinoma. METHODS The hydrodynamic injection was performed as previously described for the establishment of an AKT/c-Met-driven HCC model. To evaluate the therapeutic efficacy, orlistat(150 and 300 mg·kg;) or vehicle was intraperitoneally injected daily for 3 weeks starting 3 weeks after plasmid injection in the HCC *** mice were sacrificed 6 weeks after hydrodynamic injection. Hematoxylin and eosin staining, and Oil red O staining were applied for the pathology investigation. Immunoblotting and immunohistochemistry were applied to detect extracellular regulating protein kinase p-ERK1/2（Thr202/Tyr204）, proliferating cell nucleus antigen（PCNA）, the G;/S-specific protein cycle-D1（Cyclin D1） proliferation related protein expression and detection of PTEN and p-AKT（Thr308）, p-AKT（Ser473）, SREBP-1, FASN from the de novo lipogenic pathway-related prote

关键词： orlistat hepatocarcinogenesis fatty acid synthase proliferation lipogenesis

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Immunobiology of hepatocarcinogenesis: Ways to go or almost there?

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World Journal of Gastrointestinal Pathophysiology 2016年第3期7卷 242-255页

作者： Pavan Patel Steven E Schutzer Nikolaos Pyrsopoulos Department of Medicine Rutgers-New Jersey Medical School Division of Gastroenterology and Hepatology Rutgers-New Jersey Medical School

Hepatocellular carcinoma is on the rise and occurs in the setting of chronic liver disease and *** treatment modalities are available,mortality from this cancer remains *** therapy with the utilization of biologic compounds such as the Food and Drug Administration approved sorafenib might be the only option that can increase ***,with modern pharmacologic developments,is a new frontier in cancer therapy and therefore the immunobiology of hepatocarcinogenesis is under *** review will discuss current concepts of immunobiology in hepatocarcinogenesis along with current treatment modalities employing *** tumor microenvironment along with a variety of immune cells coexists and interplays to lead to *** infiltrating lymphocytes including CD8+ T cells,CD4+ T cells along with regulatory T cells,tumor associated macrophages,tumor associated neutrophils,myeloid derived suppressor cells,and natural killer cells interact to actively provide anti-tumor or pro-tumor ***,oncogenic pathways such as Raf/mitogenactivated protein kinase/extracellular-signal-regulated kinase pathway,phosphatidyl-3-kinase/AKT/mammalian target or rapamycin,Wnt/β-catenin,nuclear factor-κB and signal transducers and activators of transcription 3 may lead to activation and proliferation of tumor cells and are also considered cornerstones in *** directed at this complex milieu of cells has been showned to be successful in cancer *** use of vaccines,adoptive cell therapy and immune checkpoint inhibitor modulation are current options for *** translational research will shed light to concepts such as anti-tumor immunity which can add another alternative in the therapeutic armamentarium.

关键词： hepatocarcinogenesis Adoptive cell therapy Tumorigenesis Hepatocellular carcinoma Immunology Tumorigenesis Immunotherapy Immunobiology Immune checkpoint inhibitors

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Role of β-catenin in hepatocarcinogenesis of rats

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Hepatobiliary & Pancreatic Diseases International 2006年第1期5卷 85-89页

作者： Qi-Ming Wang, Kai-Ming Yang, Hong-Ying Zhou, Zhen-Hai Yu, Xiao Li and Hui-Jun Yang Department of Human Anatomy, Huaxi Medical Centre of Sichuan University and Department of Radiology, West China Hospital of Sichuan University Chengdu 610041, China Department of Human Anatomy Huaxi Medical Centre of Sichuan University Chengdu 610041 China. wangqiming-6@***

BACKGROUND: β-catenin has two distinct roles in E-cadherin mediated cell adhesion and carcinogenesis by activating the wnt/β-catenin signaling pathway. One occurs at the cell-adhesion site, where cadherins are linked to the actin-based cytoskeleton. The other takes place in the cytoplasm and nuclei and is thought to regulate cell transformation. We studied the role of β-catenin in hepatocarcinogenesis of rats. METHODS: Fresh liver specimens were obtained from normal rats. and atypical hyperplasia livers and hepatocarcinoma tissues from model rats. The changes of β-catenin in gene expression levels were detected by reverse transcriptase polymerase chain reaction (RT-PCR) in the different specimens separately. At the same time, their localization was observed immunohistochemically. RESULTS: In the normal liver specimens, β-catenin staining was seen in the cell membrane. In liver specimens of atypical byperplasia, β-catenin staining occurred in the cell cytoplasm of some cells as well as in the cell membrane of others. Immunohistochemically cancerous tissues showed the presence of β-catenin in the cytoplasm and nuclei. RTPCR revealed that the gene expression levels of β-catenin were same in all samples. CONCLUSIONS: The accumulation of β-catenin in the cytoplasm and/or nuclei frequently occurs in hepatocarcinogenesis of rats. It may be an early event in the development of hepatocarcinoma of rats.

关键词： wnt signal β-catenin hepatocarcinogenesis

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Contributions of transgenic mouse studies on the research of hepatitis B virus and hepatitis C virus-induced hepatocarcinogenesis

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World Journal of Hepatology 2015年第28期7卷 2834-2840页

作者： Shogo Ohkoshi Haruka Hirono Kazuhiko Watanabe Katsuhiko Hasegawa Masahiko Yano Department of Internal Medicine School of Life Dentistry at Niigata the Nippon Dental University Division of Gastroenterology and Hepatology Graduate School of Medical and Dental Sciences Niigata University

Transgenic mouse technology has enabled the investigation of the pathogenic effects, including those on development, immunological reactions and carcinogenesis, of viral genes directly in living organism in a real-time manner. Although viral hepatocarcinogenesis comprises multiple sequences of pathological events, that is, chronic necroinflammation and the subsequent regeneration of hepatocytes that induces the accumulation of genetic alterations and hepatocellular carcinoma(HCC), the direct action of viral proteins also play significant roles. The pathogenesis of hepatitis B virus X and hepatitis C virus(HCV) core genes has been extensively studied by virtue of their functions as a transactivator and a steatosis inducer, respectively. In particular, the mechanism of steatosis in HCV infection and its possible association with HCC has been well studied using HCV core gene transgenic mouse models. Although transgenic mouse models have remarkable advantages, they are intrinsically accompanied by some drawbacks when used to study human diseases. Therefore, the results obtained from transgenic mouse studies should be carefully interpreted in the context of whether or not they are well associated with human pathogenesis.

关键词： Transgenic mouse hepatocarcinogenesis Hepatitis C virus Hepatitis B virus X Hepatitis B virus Hepatitis C virus core protein Steatosis

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