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Genistein inhibits invasive potential of human hepatocellular carcinoma by altering cell cycle, apoptosis, and angiogenesis

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World Journal of Gastroenterology 2005年第41期11卷 6512-6517页

作者： Yan Gu Chen-Fang Zhu Hitoshi Iwamoto Ji-Sheng Chen Department of General Surgery The Ninth People's Hospital Shanghai Second Medical UniversityShanghai 200011 China Fifth Department of Surgery Tokyo Medical University Tokyo 193-8639 Japan Department of Hepatobiliary Surgery Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China

AIM： To study the in vitro and in vivo inhibitory effects of genistein on invasive potential of Bel 7402 hepatocellular carcinoma （HCC） cells and to explore the underlying mechanism. METHODS： Bel 7402 HCC cells were exposed to genistein. The invasive activity of tumor cells was assayed in transwell cell culture chamber, p125^FAK expression and cell cycle were evaluated by a functional assay. Cell apoptosis analysis was performed with TUNEL method. In addition, bilateral subrenal capsule xenograft transplantation of HCC was performed in 10 nude mice. Genistein was injected and the invasion of HCC into the renal parenchyma was observed. Nicrovessels with immunohistochemical staining were detected. RESULTS： Genistein significantly inhibited the growth of Bel 7402 cells, the inhibitory rate of tumor cells was 26 -42%. The invasive potential of Bel 7402 cells in vitro was significantly inhibited, the inhibitory rate was 11- 28%. Genistein caused G2/M cell cycle arrest, S phase decreased significantly. The occurrence of apoptosis in genistein group increased significantly. The expression of p125^FAK in 5 μg/mL genistein group （15.26±0.16%） and 10 μg/mL genistein group （12.89±0.36%） was significantly lower than that in the control group （19.75± 1.12%, P〈0.05）. Tumor growth in genistein-treated nude mice was significantly retarded in comparison to control mice, the inhibitory rate of tumor growth was about 20%. Genistein also significantly inhibited the invasion of Bel 7402 cells into the renal parenchyma of nude mice with xenograft transplant. The positive unit value of microvessels in genistein-treated group （10.422 ±0.807） was significantly lower than that in control group （22.330 ± 5.696, P〈 0.01）. CONCLUSION： Genistein can effectively inhibit the invasive potential of Bel 7402 HCC cells by altering cell cycle, apoptosis and angiogenesis, inhibition of focal adhesion kinase may play a significant role in this process.

关键词： Genistein human hepatocellular carcinoma Invasion Cell cycle Apoptosis Angiogenesis

Inhibitory effects of genistein on metastasis of human hepatocellular carcinoma

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World Journal of Gastroenterology 2009年第39期15卷 4952-4957页

作者： Yan Gu Cheng-Fang Zhu Ya-Lei Dai Qiang Zhong Bo Sun Department of General Surgery Shanghai Ninth Hospital Shanghai Jiao Tong University School of Medicine Shanghai 200011 China Department of Immunology Tongji University School of Medicine Shanghai 200092 China

AIM： To investigate the inhibitory effects of genistein on metastasis of MHCC97-H hepatocellular carcinoma cells and to explore the underlying mechanism. METHODS： MHCC97-H hepatocellular carcinoma cells were exposed to genistein. A cell attachment assay was carried out in a microculture well pre-coated with fibronectin. The invasive activity of tumor cells was assayed in a transwell cell culture chamber, and cell cycle and apoptosis were evaluated by a functional assay. In addition, the expression and phosphorylation of FAK were detected by Western blotting. In situ xenograft transplantation of hepatocellular carcinoma was performed in 12 nude mice and lung metastasis of hepatocellular carcinoma was observed. RESULTS： Genistein significantly inhibited the growth of MHCC97-H cells in vitro. Adhesion and invasiveness of MHCC97-H cells were inhibited in a concentrationdependent fashion, and the inhibitory effect of genistein was more potent in the 10 i^g/mL and 20 i^g/ mL genistein-treated groups. Genistein caused G0/G1 cell cycle arrest, an S phase decrease, and increased apoptosis. The expression and phosphorylation of FAK in MHCC-97H cells were significantly decreased. In situ xenograft transplantation of hepatocellular carcinoma was also significantly suppressed by genistein. The number of pulmonary micrometastatic loci in the genistein group was significantly lower compared with the control group （12.3 ± 1.8 vs 16.6± 2.6, P 〈 0.05）. CONCLUSION： Genistein appears to be a promising agent in the inhibition of metastasis of hepatocellular carcinoma.

关键词： human hepatocellular carcinoma Genistein Metastasis

Enhanced radioimmunotherapeutic efficacy of a monoclonal antibody cocktail against SMMC-7721 human hepatocellular carcinoma

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Cell Research 1998年第3期8卷 241-247页

作者： SONG YI QIANG GEN FENG WANG XIN LAN DAI HONG XIE(Shanghai Institute of Cell Biology, Chinese Academy of Sciences, Shanghai 200031, China) Shanghai Institute of Cell Biology Chinese Academy of Sciences Shanghai China

The improved tumoricidal effect of the radioatibody mixture ("cocktail") has been reported recently for the treatment of colon tumor. In the present study, we demonstrated the enhanced radioimmunotherapeutic efficacy of a monoclonal atibody (MAb) cocktail against human hepatocellular carcinoma. Therapeutic efficacy was determined by measuring the change in tumor size over a period, determining the percentage of growth inhibition of each treatment at various times after radioantibody therapy. boioimmunotherapy of SMMC-7721 human hepatoma xenografts in athymic nude mice with combination of 131I labeled Hepama-1 and 131Llabeled 9403 mouse MAbs was more effective than using either Hepeam-1 or 9403 Mab alone The MAb cocktail could target a greater number of hepstoma cells and increase the magnitude of hepatoma cen uptde of radioamibodies. The in vjtro results explain the enhanced effect of the MAb cocktail in in vjvo model system.

关键词： Mouse monoclonal antibody human hepatocellular carcinoma radioimmunotherapy antibody cocktail

Preliminary Study of Oxidative Stress in human hepatocellular carcinoma and Adjacent Normal Liver Tissues

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Chinese Journal of Clinical Oncology 2006年第1期3卷 11-14页

作者： Hongwei Yu Chunying Chen Jiangxue Wang Yuxi Gao Guilong Deng Yingbin Liu Shuyou Peng Zhifang Chai Key Laboratory of Nuclear Analysis Techniques Institute of High Energy Physics Chinese Academy of Sciences Beijing 100049 China Department of General Surgery the Second Affiliated Hospital School of Medicine Zhejiang University Hangzhou 310009 China

OBJECTIVE The antioxidative system in human hepatocellular carcinoma was investigated. METHODS The activities of cytosolic catalase (CAT), superoxide dismu-tase, glutathione peroxidase (GSH-Px), glutathione S-tranferase and levels of reduced glutathione, total protein thiols and malondialdehyde were assayed in 10 cases of hepatocellular carcinoma and adjacent normal liver. RESULTS Hepatoma tissues showed higher activities of CAT, GSH -Px and lower content of total antioxidative capacity compared to adjacent normal liver tissue (P<0.05). CONCLUSION These findings suggest that the antioxidative defense-related enzymes and antioxidants are largely regulated in hepatoma cells. However, the mechanism which is not clear requires further investigation.

关键词： human hepatocellular carcinoma antioxidative enzymes oxidative stress.

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Farnesoid X receptor expression is reduced in human hepatocellular carcinoma

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Journal of Medical Colleges of PLA(China) 2012年第1期27卷 1-9页

作者： Zhang Wenyu Chen Ping Zhao Yuanyin Lou Guiyu Department of Endocrinology People's Hospital of ZhengzhouZhengzhou 450003China Department of Hepatobiliary Surgery Daping Hospital Institute of Surgery ResearchThird Military Medical UniversityChongqing 400042China Department of Biochemistry College of Basic Medical SciencesThird Military Medical UniversityChongqing 400038China

Farnesoid X receptor (FXR, NR1H4) is a member of nuclear hormone receptor superfamily. Previously studies showed that FXR-/- mice spontaneously developed liver tumors when they aged, however, the relevance of which to human hepatocellular carcinoma (HCC) is unclear. The aim of this study is to observe whether FXR expression is also downregulated in HCC and discuss the mechanism of the reduced FXR expression in HCC. Expression of FXR and small heterodimer partner (SHP) was measured by real-time PCR and immunohistochemical technique. Effect of pro-inflammatory cytokines on expression of FXR and its promoter activity were determined in primary hepatocytes or HepG2 and Huh7 cell lines. Our results showed that expression of FXR and its target gene SHP in human HCC was strongly downregulated compared to the normal liver tissues. In addition, pro-inflammatory cytokines were able to decrease FXR expression by inhibiting the FXR promoter activity. In conclusion this work demonstrates FXR expression is strongly downregulated in human HCC, which may be caused by decreased FXR promoter activity, suggesting a potential role of FXR in human HCC development.

关键词： Farnesoid X receptor human hepatocellular carcinoma Pro-inflammatory cytokines

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Targeted depletion of vigilin via lentiviral shRNA inhibitor causes growth inhibition of human hepatocellular carcinoma cells and suppresses tumor development and/or progression in vivo

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Targeted depletion of vigilin via lentiviral shRNA inhibitor...

The study of anti-hepatitis drug dimethyl dicarboxylate biphenyl on invasion of human hepatocellular carcinoma MHCC97-H cells and its active mechanisms

中国生物化学与分子生物学会第十届会员代表大会暨全国学术会议

作者： Wenli Yang Wenqing Huang Ling Wei Shuwang Duan Junhong Li Yang Qin Department of Biochemistry and Molecular Biology School of Preclinical and Forensic MedicineWest China Medical Center

hepatocellular carcinoma(HCC),one of the most lethal forms of tumors in the world,causing more than 600,000 deaths per year,remains resistant to currently available *** is a conserved protein,consisting of 14 tandem and related hnRNP K homology(KH) domains, among the conserve amino acids,vigilin domains 1 and 3 show the sequence *** previously demonstrated that the overexpression of vigilin was in human epithelial ovarian cancer cell line TOV-112D and human prolactinomas, enlightening a novel mechanism involved and targetbased approaches could be developed for application in the

关键词： vigilin human hepatocellular carcinoma short hairpin RNA(shRNA) lentivirus interference apoptosis proliferation tumorigenesis

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The Chinese-German Journal of Clinical Oncology 2008年第1期7卷 2-6页

作者： Hua Sun Gengtao Liu Department of Pharmacology Institute of Materia Medica Peking Union Medical College ＆ Chinese Academy of Medical Sciences Beiiing 100050 China

Objective： To assess the anti-invasive effect of DDB and its possible active mechanism in human hepatocellular carcinoma MHCC97-H with high metastasis potential. Methods： MTT assay was used to evaluate the cytotoxicity of DDB to MHCC97-H cells and the anti-adhesion of DDB on MHCC97-H cells to laminin （LN） and fibronectin （FN）. The anti-invasive effect of DDB was detected by the transwell chamber experiment. VEGF, nm23-H1 and uPAR mRNA transcriptions were determined by RT-PCR assay. The secretion and expression of a-fetal protein （AFP） were analyzed by ELISA and flow cytometry, respectively. Results： DDB at non-cytotoxic concentrations （10, 50 and 100 μmol/L） obviously inhibited the adhesion of MHCC97-H on LN and FN. In the transwell chamber experiment, the inhibition rates of the invasion of DDB 50 and 100 μmol/L on MHCC97-H cells were 25.8% and 32.3%, respectively. By RT-PCR assay, DDB 50 and 100 μmol/L decreased VEGF, nm23-H1 and uPAR mRNA expressions in MHCC97-H cells. The ELISA assay showed that 50, 100 and 200 μmol/L DDB decreased the AFP secretion of MHCC97-H cells, the inhibitory rates were 16.5%, 17.5% and 48.5%, respectively. DDB also decreased the expression of AFP in MHCC97-H cells by flow cytometry assay. Conclusion： DDB, an anti-hepatitis drug, at non-cytotoxic concentrations showed significant anti-invasion effect in human hepatocellular carcinoma MHCC97-H cells, and the inhibition of VEGF, nm23-H1 and uPAR expression should contribute to the anti-invasion property of DDB.

关键词： dimethyl dicarboxylate biphenyl human hepatocellular carcinoma MHCC97-H cell invasion metastasis

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Effects of sargentgloryvine stem extracts on HepG-2 cellsin vitro andin vivo

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World Journal of Gastroenterology 2011年第23期17卷 2848-2854页

作者： Ming-Hua Wang Min Long Bao-Yi Zhu Shu-Hui Yang Ji-Hong Ren Hui-Zhong Zhang Department of LaboratoryMedicine and Research Center Tangdu Hospital Fourth MilitaryMedical University Xi＇an 710038 Shaanxi Province China

AIM:To observe the effects of sargentgloryvine stem extracts (SSE) on the hepatoma cell line HepG-2 in vitro andin vivo and determine its mechanisms of ***:Cultured HepG-2 cells treated with SSE were analysed by 3-(4,5-Dimethyl-thiazol-2-yl)-2,5Diphenyltetrazolium bromide and clone formation *** cell cycle and apoptosis analysis were conducted by flow cytometric,TdT-Mediated dUTP Nick End Labeling and acridine orange/ethidium bromide staining methods,and protein expression was examined by both reverse transcriptase-polymerase chain reaction and Western *** pathological changes of the tumor cells were observed by haematoxylin and eosin *** growth inhibition and side effects were determined in a xenograft mouse ***:SSE treatment could not only inhibit HepG-2 cell proliferation in a doseand time-dependent manner but also induce apoptosis and cell cycle arrest at the S *** number of colonies formed by SSEtreated tumor cells was fewer than that of the controls (P0.05).Systemic administration of SSE could inhibit the HepG-2 xenograft tumor growth with no obvious toxic side effects on normal ***:SSE can induce apoptosis of HepG-2 cells in vitro and in vivo through decreasing expression of Bcl-xl and Mcl-1 and increasing expression of Bax.

关键词： Sargentgloryvine stem extract Apoptosis human hepatocellular carcinoma HepG-2 Bcl-2 family

Murine double minute gene 2(MDM2)promoted hepatocellular carcinoma(HCC)cell growth by targeting fructose-1,6-bisphosphatase(FBP1)for degradation

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BIOCELL 2022年第6期46卷 1483-1491页

作者： YAO XU BIN WU JING YANG SHENG ZHANG LONGGEN LIU SUOBAO XU JIAKAI JIANG Department of Intensive Care Unit Changzhou No.3 People’s HospitalChangzhou213000China Department of General Surgery Changzhou No.3 People’s HospitalChangzhou213000China Department of Gastroenterology Changzhou No.1 People’s HospitalChangzhou213000China Department of Liver Disease Changzhou No.3 People’s HospitalChangzhou213000China

To study the roles and association of murine double minute gene 2(MDM2)and fructose-1,6-biphosphatase(FBP1)in human hepatocellular carcinoma(HCC),growth response of human HCC cells was assessed using proliferation and apoptosis ***-survival AKT signaling associated proteins(p-AKT,survivin and cleaved caspase 3)were assessed using western *** correlation between MDM2 and FBP1 was assessed using coimmunoprecipitation combined with ubiquitination *** data suggested that low expression of FBP1 was correlated with high levels of MDM2 in HCC cell lines(Huh7 and Hep3B).Overexpression of FBP1 resulted in antiproliferation,pro-apoptosis,the up-regulation of cleaved caspase 3 while the downregulation of survivin and phosphor(p)-AKT,however,knockdown of FBP1 led to the ***,overexpression of MDM2 potently reversed FBP1-induced proliferation inhibition and apoptosis,while Nutlin-3(an MDM2 inhibitor)reversed the change trends induced by FBP1 knockdown in the aforementioned ***,but not least importantly,our data elucidated that MDM2 binds directly to FBP1 and promotes FBP1 *** conclusion,our data firstly suggested the involvement of FBP1 and its association with MDM2 in HCC cell ***2-FBP1-regulated HCC cell growth and the activation of AKT were mediated,at least in part,through FBP1 degradation.

关键词： human hepatocellular carcinoma MDM2 FBP1 FBP1 ubiquitination