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Novel diagnosis and therapy for hepatoma targeting HBV-related carcinogenesis through alternative splicing of FIR (PUF60)/FIRΔexon2

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Hepatoma Research 2018年第9期4卷 142-158页

作者： Kazuyuki Matsushita Tyuji Hoshino Department of Laboratory Medicine&Division of Clinical Genetics and Proteomics Chiba University HospitalChiba260-8677Japan Department of Physical Chemistry Chiba UniversityChiba 260-8670Japan

Aim: Disturbed alternative splicing of far upstream element-binding protein-interacting repressor (FIR) was found to be unable to repress c-Myc transcription and so it might be important for suppressing tumor development. FIR is a splicing variant of poly (U)-binding-splicing factor (PUF60), and forms complex with other splicing factors. FIR/PUF60 is a splicing factor of U2 small nuclear ribonucleoprotein auxiliary factor family, Thus FIR/PUF60 is a multifunctional protein. The expression of exon2-lacking splicing variant of FIR, FIRΔexon2, is elevated in many cancer tissues and promotes tumor development by disabling FIR-repression to sustain c-Myc activation. FIRΔexon2, as a dominant negative of FIR, opposed apoptosis in cancer cells. FIR/FIRΔexon2 interacts with degron pocket of F-box and W (Typ) D (Asp) repeat domain-containing 7 and inhibits proteolysis of substrates proteins. Recently, FIR/PUF60 was identified as a versatile regulator of transcriptional and post-transcriptional steps in expression of hepatitis B virus (HBV) pregenomic RNA (pgRNA) expression. Methods: Small molecular chemical compounds against FIR and FIRΔexon2 were screened among 2,3275 chemicals by natural product depository array (RIKEN, Wako, Saitama, Japan). Results: Nine chemicals against FIR and four chemicals against FIRΔexon2 were identified as candidates of interacting chemicals. Interestingly, BK697 contains WD -like structure. Among them, BK697 against FIRΔexon2 inhibited hepatoma cell growth. Conclusion: Therefore, FIR (PUF60)/FIRΔexon2 is multifunctional and applicable for clinical use for HBV suppression and hepatoma treatment. Together, one clue to the development of hepatome diagnosis and therapies directed against FIR/FIRΔexon2/PUF60 with small molecular weight chemicals that inhibit HBV cccDNA replication.

关键词： Hepatocellular carcinoma hepatitis B virus covalently closed circular DNA far upstream element-binding protein-interacting repressor poly (U)-binding-splicing factor F-box and W (Typ) D (Asp) repeat domain-containing 7 natural product depository array U2A

PNPLA3 I148M polymorphism and progressive liver disease

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World Journal of Gastroenterology 2013年第41期19卷 6969-6978页

作者： Paola Dongiovanni Benedetta Donati Roberta Fares Rosa Lombardi Rosellina Margherita Mancina Stefano Romeo Luca Valenti Internal Medicine Fondazione IRCCS Ca’ Granda Ospedale Policlinico MilanoDepartment of Pathophysiology and TransplantationUniversità degli Studi di Milano20122 MilanoItaly Sahlgrenska Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory Department of Molecular and Clinical MedicineUniversity of Gothenburg40530 GothenburgSweden Clinical Nutrition Unit Department of Medical and Surgical SciencesUniversity Magna Graecia88100 CatanzaroItaly

The 148 Isoleucine to Methionine protein variant(I148M)of patatin-like phospholipase domain-containing 3(PNPLA3),a protein is expressed in the liver and is involved in lipid metabolism,has recently been identified as a major determinant of liver fat *** studies confirmed that the I148M variant predisposes towards the full spectrum of liver damage associated with fatty liver:from simple steatosis to steatohepatitis and progressive ***,the I148M variant represents a major determinant of progression of alcohol related steatohepatitis to cirrhosis,and to influence fibrogenesis and related clinical outcomes in chronic hepatitis C virus hepatitis,and possibly chronic hepatitis B virus hepatitis,hereditary hemochromatosis and primary sclerosing *** in all,studies suggest that the I148M polymorphism may represent a general modifier of fibrogenesis in liver ***,the effect of the I148M variant on fibrosis was independent of that on hepatic steatosis and inflammation,suggesting that it may affect both the quantity and quality of hepatic lipids and the biology of non-parenchymal liver cells besides hepatocytes,directly promoting ***,PNPLA3 is a key player in liver disease *** of the I148M polymorphism will possibly inform clinical practice in the future,whereas the determination of the effect of the 148M variant will reveal mechanisms involved in hepatic fibrogenesis.

关键词： Alcoholic liver disease Chronic hepatitis C virus hepatitis Fibrogenesis Genetics Hepatocellular carcinoma Liver disease Nonalcoholic fatty liver disease Patatin-like phospholipase domain-containing 3 Single nucleotide polymorphism Steatosis

KCTD-12 inhibits the in vitro proliferation and invasion of gastrointestinal stromal tumor cells: the experimental study

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Journal of Hainan Medical University 2017年第12期23卷 8-11页

作者： Juan-Fang Wang Jian-Ping Niu Internal Medicine Department No.2 Ganquan County Hospital in Shaanxi ProvinceYan'an716100China Department of Gastroenterology Shaanxi Provincial People's HospitalXi'an710068China

Objective:To study the effects of potassium channel tetramerization domain-containing 12 (KCTD-12) overexpression on in vitro proliferation and invasion of gastrointestinal stromal tumor ***:Gastrointestinal stromal tumor cell lines were cultured and randomly divided into KCTD-12 overexpression group and NC overexpression group that were transfected with KCTD-12 overexpression plasmid and negative control plasmid respectively. 24 h after transfection, the expression of proliferation genes, apoptosis genes, PI3K and p38MAPK signaling pathway molecules as well as invasion genes in cells were detected. Results: Ki-67, SCIN, Bcl-2, p-PI3K, p-AKT, p-p38MAPK, CD146, PAR-2, SDF-1 and CXCR4 expression in KCTD-12 overexpression group were significantly lower than those in NC overexpression group while Bax, Caspase-3, Caspase-7, Caspase-9 and p-FOXO1 expression were significantly higher than those in NC overexpression ***:KCTD-12 can inhibit the in vitro proliferation and invasion of gastrointestinal stromal tumor cells.

关键词： Gastrointestinal stromal tumor Potassium channel tetramerization domain-containing 12 Proliferation Invasion

Insulin resistance and steatosis in HBV-HCV co-infected patients: Role of PNPLA3 polymorphisms and impact on liver fibrosis progression

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World Journal of Hepatology 2014年第9期6卷 677-684页

作者： Rosa Zampino Adriana Boemio Aldo Marrone Luciano Restivo Maria Chiara Fascione Riccardo Nevola Luigi Elio Adinolfi Nicola Coppola Carmine Minichini Mario Starace Evangelista Sagnelli Grazia Cirillo Emanuele Miraglia del Giudice Maria Stanzione Emanuele Durante-Mangoni Giovanna Salzillo Department of Medical SurgicalNeurologicalMetabolicand GeriatricSciencesSecond University of Naples80100 NaplesItaly Clinical Hospital of Marcianise ASL Caserta81025 Marcianise (CE)Italy Department of Medical SurgicalNeurologicalMeta-bolicand GeriatricSciencesSecond University of Naples80100 NaplesItaly Department of Mental Health and Public Medicine Section of Infectious DiseasesSecond University of Naples80100 NaplesItaly Department of Pediatrics Second University of Naples80100 NaplesItaly Department of Clinical and Experimental Medicine and Surgery "F. Magrassi e A. Lanzara"Second University of Naples80100 NaplesItaly Internal Medicine Monaldi Hospital Second University of 80100 NaplesItaly

AIM:To evaluate steatosis,insulin resistance(IR)and patatin-like phospholipase domain-containing 3(PNPLA3) and their relation to disease progression in hepatitis B and C viruses(HCV-HBV) coinfected ***:Three hundred and thirty patients with biopsy proven chronic hepatitis were enrolled:66 had HBV-HCV,66 HBV and 198 HCV *** of steatosis,IR and PNPLA3 polymorphisms and their relation to anthropometric,biochemical,virological and histological parameters were ***:Prevalence of steatosis in group HBV-HCV was similar to that in HCV(47.0% vs 49.5%,respec-tively);group HBV showed the lowest steatosis(33.3%).Group HBV-HCV had a lesser degree of steatosis than HCV(P = 0.016),lower HCV RNA levels(P = 0.025) and lower prevalence and degree of IR(P = 0.01).PNPLA3 polymorphisms were associated with *** HBV-HCV showed higher levels of liver fibrosis than group HCV(P = 0.001),but similar to that ob-served in HBV *** HBV-HCV group,liver fibrosis was not associated with steatosis,IR or *** infection was the independent predictor of advanced liver ***:HBV-HCV co-infected patients have lower degree of hepatic steatosis,IR and HCV RNA than HCV mono-infected;co-infected patients showed a more rapid liver fibrosis progression that seems to be due to the double infection and/or HBV dominance.

关键词： Steatosis Insulin resistance Hepatitis B and C viruses co-infection Patatin-like phospholipase domain-containing 3 Liver fibrosis

乳腺癌组织中IGF-IR、SUSD3的表达及其临床意义

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临床肿瘤学杂志 2014年第4期19卷 303-306页

作者：于正洪王新星石亚琴顾军姜恩泽余波张新华陈龙邦第二军医大学南京临床医学院南京军区南京总医院肿瘤内科南京210002 南京军区南京总医院呼吸内科 210002 南京军区南京总医院普通外科 210002 南京军区南京总医院病理科 210002

目的探讨胰岛素样生长因子-I受体(IGF-IR)和SUSD3在乳腺癌组织中的表达情况,分析两者与临床病理特征的关系及其两者间的相关性。方法采用Max VisionTM免疫组化法检测100例乳腺癌组织和对应癌旁组织中IGF-IR、SUSD3的表达,并分析其与乳... 详细信息

目的探讨胰岛素样生长因子-I受体(IGF-IR)和SUSD3在乳腺癌组织中的表达情况,分析两者与临床病理特征的关系及其两者间的相关性。方法采用Max VisionTM免疫组化法检测100例乳腺癌组织和对应癌旁组织中IGF-IR、SUSD3的表达,并分析其与乳腺癌临床病理特征的关系。结果 IGF-IR在乳腺癌和癌旁组织中的阳性表达率分别为86.0%和3.0%(P0.05)。IGF-IR和SUSD3在乳腺癌组织中的表达呈正相关(r=0.553,P<0.01)。结论 IGF-IR、SUSD3可能与乳腺癌的发生、发展有关,与ER联合检测对判断乳腺癌预后和指导术后辅助治疗有重要意义。

关键词：乳腺癌胰岛素样生长因子-I受体 SUSD3 雌激素受体 Insulin-like growth factor-I receptor (IGF-IR) Sushi domain-containing protein 3 (SUSD3)

HBsAg对健康成人外周血单核细胞来源树突状细胞Tim-3信号通路的影响

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浙江医学 2015年第11期37卷 916-919页

作者：余真君汤永志燕飞朱敏朱坚胜温州医科大学附属台州医院感染科临海317000 温州医科大学附属台州医院公共科研平台临海317000

目的探讨HBsAg对健康成人外周血单核细胞来源树突状细胞(MD—DCs)的免疫活性及对T细胞免疫球蛋白黏蛋白分子3(Tim-3)和下游信号分子核因子-κB(NF—κB)蛋白表达的影响。方法分离健康成人外周血单核细胞,经GM—CSF、IL-4联合诱导为树突... 详细信息

目的探讨HBsAg对健康成人外周血单核细胞来源树突状细胞(MD—DCs)的免疫活性及对T细胞免疫球蛋白黏蛋白分子3(Tim-3)和下游信号分子核因子-κB(NF—κB)蛋白表达的影响。方法分离健康成人外周血单核细胞,经GM—CSF、IL-4联合诱导为树突状细胞(DCs),流式细胞术检测DCs表面标志物表达水平。MD—DCs分4组添加不同浓度HBsAg(0、1、2、5μg/ml),分别设为对照组、+1μg/ml组、+2μg/ml组、+5μg/nl组,Western印迹法检测Tim-3、NF—κB信号蛋白表达,细胞增殖与毒性检测试剂检测MD—DCs刺激同种异体淋巴细胞增殖的能力,ELISA法检测细胞因子分泌水平。结果外周血来源单核细胞成功诱导分化为DCs。与对照组相比,+2μg/ml及+5μg/ml组MD—DCs Tim-3及NF—κB表达水平均上调,刺激同种异体T淋巴细胞增殖能力均增强,炎症因子IL-6、IL-10、IFN—γ分泌水平均增高(均P0.05)。与其他3组相比,+5μg/ml组MD—DCs Tim-3、NF—κB、炎症因子分泌水平增高,刺激同种异体淋巴细胞增殖能力增强(均P<0.05)。结论 HBsAg上调MD—DCs Tim-3及NF—κB表达水平,增强MD—DCs免疫活性,且刺激作用随HBsAg浓度的增高而增强。

关键词：树突状细胞肝炎表面抗原,乙型 T细胞免疫球蛋白黏蛋白分子3 T cell immunoglobulin and mucin domain-containing molecules-3