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| 1 | Experimental study of anti-tumor effects of polysaccharides from Angelica sinensis显示文摘AIM: To investigate the in vivo anti-tumor effects of total polysaccharide (AP-0) isolated from Angelica sinensis (Oliv.)Diels (Danggui) on mice and thein vitro inhibitory effects of AP-0 and its sub-constituents (AP-1, AP-2 and AP-3) on invasion and metastasis of human hepatocellular carcinoma.METHODS: Three kinds of murine tumor models in vivo,sarcoma 180 (S180), leukemia L1210 and Ehrlich ascitic cancer (FAC) were employed to investigate the anti-tumor effects of AP-0. For each kind of tumor model, three experimental groups were respectively given AP-0 at doses of 30, 100 and 300 mg/kg byip once a day for 10 days.Positive control groups were respectively given Cy at a dose of 30 mg/kg for S180 and leukemia L1210, and 5-FU at a dose of 20 mg/kg for EAC. On d 11, mice bearing S180were sacrificed and the masses of tumors, spleens and thymus were weighed. The average living days of mice bearing EAC and of mice bearing L1210 were observed,and the rates of life prolongation of each treatment were calculated, respectively. The inhibitory effects of APs on hepatoma invasion and metastasis in vitro were investigated by employing human hepatocellular carcinoma cell line (HHCC) with the Matrigel invasion chamber, adhesion to extracelluler matrix and chemotatic migration tests, respectively.RESULTS: AP-0 had no obviously inhibitory effect on the growth of S180, but it could significantly decrease the thymus weights of the mice bearing S180. AP-0 could significantly reduce the production of ascitic liquids and prolong the life of mice bearing EAC. AP-0 could also increase the survival time of mice bearing L1210. AP-0 and AP-2 had significantly inhibitory effects on the invasion of HHCC into the Matrigel reconstituted basement membrane with the inhibitory rates of 56.4% and 68.3%, respectively. AP-0, AP-1, AP-2 and AP-3 could influence the adhesion of HHCC to extracellular matrix proteins (Matrigel and fibronectin) at different degrees, among them only AP-3 had significant blocking effect on the adhesion of HHCC to fibronectin with an inhibitory rate of 30.3%. AP-0, AP-1 and AP-3 could partially inhibit the chemotactic migration abilities of HHCC.CONCLUSION: The experimental findings suggest that total polysaccharide of Angelica sinensis (Oliv.) Diels (Chinese Danggui) possesses anti-tumor effects on experimental tumor models in vivo and inhibitory effects on invasion and metastasis of hepatocellular carcinoma cells in vitro. | Wen-MingZhao Zhi-NanChen PengShang Ai-RongQian Tie-HongYang MinJia Qi-BingMei Chi-HinCho | 2003 | World Journal of Gastroenterology2003，9，9： | 27 |
| 2 | Inhibitory effects of antisense RNA of HAb18G/CD147 on invasion of hepatocellular carcinoma cells in vitro显示文摘AIM: To study the inhibitory effects of antisense RNA of HAb18G/CD147 on invasion of hepatocellular carcinoma (HCC) cells in vitro.METHODS: Antisense RNA of HAb18G/CD147 vector PCIasHAb18G was constructed by reversely inserting HAb18G/CD147 cDNA to eukaryotic expression vector PCI-neo. The HCC cell line HHCC was transfected by PCI-asHAb18G via cation liposome. Expression of HAb18G/CD147 of transfected cells selected by G418 (geneticin) was observed by immunohistochemical SP staining and FACS (fluorescence activated cell sorting). Gelatin zymography was used to determine the effect of PCI-asHAb18G on reducing secretions of MMP2 and MMP-9 of the transfected cells. Boyden chamber was employed to test the invasion of HCC cells in vitro.RESULTS: The construction of antisense RNA vector PCIasHAb18G was verified correct by partial nucleotide sequencing and restricted endonuclease digestion. The expression of HAb18G/CD147 in transfected HHCC was inhibited by PCI-asHAb18G. Secretions of MMP-2 and MMP9 of transfected HHCC were reduced and the invasion of transfected HHCC was inhibited compared to HHCC,respectively.CONCLUSION: Invasion of HCC cells can be inhibited by antisense RNA of HAb18G/CD147. HAb18G/CD147 may be used as a potential target of drugs for anti-invasion and metastasis of HCC. | Yu Li Peng Shang Ai-Rong Qian Li Wang Yong Yang Zhi-Nan Chen, Department of Cell Biology, Fourth Military Medical University, Xi’an 710032, Shaanxi Province, China | 2003 | World Journal of Gastroenterology2003，9，10： | 22 |
| 3 | Alpha-fetoprotein stimulated the expression of some oncogenes in human hepatocellular carcinoma Bel 7402 cells显示文摘AIM:To investigate the molecular mechanism of alphafetoprotein (AFP) on regulating the proliferation of human hepatocellular carcinoma cells.METHODS: Alpha-fetoprotein purified from human umbilical blood was added to cultured human hepatocellular carcinoma Bel 7402 cells in vitro for various treatment periods. The expression of c-fos, c-jun,and N-ras mRNA involved in proliferation and differentiation of cells was analyzed by Northern blot,and the expression of mutative p53 and p21^ras proteins was determined by Western blot.RESULTS:The results showed that AFP (20mg/L) stimulated mRNA expression of these oncogenes in Bel 7402 cells.The expression of c-fos mRNA increased by 51.1%,60.9%,96.0%,and 25.5% at 2, 6, 12, and 24 h, respectively.The expression of c-jun and N-ras mRNA reached to the maximum which increased by 81.3% and 59.9% as compared with the control alter 6h and 24h incubation with AFP, respectively.Western blot assay also demonstrated that AFP promoted the expression of mutative p53 and p21^ras proteins, and the increased rate of those proteins was 13.0%,39.9%, and 70.9%, as well as 35.2%, 102.6%, and 46.8% at 6, 12, and 24h,respectively, as compared with the control.Both human serum albumin (the same dosage as AFP) and monoclonal anti-AFP antibody failed to stimulate the expression of these oncogenes,but anti-AFP antibody could block the functions of AFP.CONCLUSION:The data indicate that AFP can stimulate the expression of some oncogenes to enhance the proliferation of human hepatocellular carcinoma Bel 7402 cells. | Meng-SenLi Ping-FengLi QianChen Guo-GuangDu GangLi | 2004 | World Journal of Gastroenterology2004，10，6： | 19 |
| 4 | Genes encoding Pir51,Beclin 1,RbAp48 and aldolase b are up or down-regulated in human primary hepatocellular carcinoma显示文摘AIM:To reveal new tumor markers and target genes from differentially expressed genes of primary tumor samples using cDNA microarray.METHODS: The ^33p labeled cDNAs were synthesized by reverse transcription of message RNA from the liver cancerous tissue and adjacent non-cancerous liver tissue from the same patient and used to hybridize to LifeGrid 1.0 cDNA microarray blot containing 8400 known and unique human cDNA gene targets, and an expression profile of genes was produced in one paired human liver tumor tissue.After a global analysis of gene expression of 8400 genes,we selected some genes to confirm the differential expression using Northern blot and RT-PCR.RESULTS:Parallel analysis of the hybridized signals enabled us to get an expression profile of genes in which about 500genes were differentially expressed in the paired liver tumor tissues. We identified 4 genes, the expression of three-(Beclin 1, RbAp48 and Pir51) were increased and one (aldolase b) was decreased in liver tumor tissues. In addition,the expression of these genes in 6 hepatoma cell lines was also showed by RT-PCR analysis.CONCLUSION:cDNA microarray permits a high throughput identification of changes in gene expression. The genes encoding Beclin 1, RbAp48, Pir51 and aldolase b are first reported that may be related with hepatocarcinoma. | HaiSong Shuang-LuoXia ChengLiao Yi-LiangLi Yi-FeiWang Tsai-PingLi Mu-JunZhao | 2004 | World Journal of Gastroenterology2004，10，4： | 19 |
| 5 | Effect of arsenic trioxide on rat hepatocarcinoma and its renal cytotoxicity显示文摘AIM: To study the effect of arsenic trioxide (As2O3) on rat experimental hepatocarcinoma and its renal cytotoxicity.METHODS: The hepatocarcinoma model was established by diethaylnitrosamine perfusion in stomach of 120 Wistar rats, and the treatment began at the end of 20 weeks.Before the treatment, the rat models were randomly divided into 5 groups. In the treatment groups, three doses of As2O3 were injected into rat abdominal cavity, the total time of drug administration was 4 weeks. Cisplatin control or the blank group was injected into abdominal cavity with equal amount of cisplatin or saline at the same time,respectively. On the 7th, 14th and 28th day after the treatment, the hepatocarcinoma nodules were obtained and the morphologic changes of hepatocarcinoma cells were observed under light and electron microscopes;Immunohistochemistry (S-P methods) was employed to detect the expression of bcl-2, bax and PCNA in hepatocarcinoma tissues; flow cytometry (TUNEL assay)was used to detect the apoptosis of liver cancer cells and the change of cytokinetics. On the 28th day, the kidneys were obtained and their histologic changes were observed under light microscope, and immunohistochemistry (SP stain) was also employed to detect the expression of bcl-2and PCNA. Cisplatin and saline solution were used as the control.RESULTS: As2O3 could induce the apoptosis of rat liver cancer cells and exhibited typical morphologic changes.The incidence of apoptosis of hapatocarcinoma cells was elevated (P=0.001). The elevation was the most higher in the group of middle-dose of As2O3 (1 mg.kg-1), significantly higher than that of the other arsenic groups and the controls (P=0.001). Large dose of As2O3 (5 mg.kg-1) was able to arise the incidence of apoptosis, but also produced a large amount of necrosis and inflammatory reaction. Middle dose of As2O3 dramatically increased the cell number in G2/M phase (P=0.0001), and apoptosis happened apparently.The expression of bcl-2 and bax was related to the dose of As2O3. With the up-regulation of apoptotic incidence, the ratio of bcl-2/bak decreased. But the incidence of apoptosis was not the highest status and the ratio of bcl-2/bax was at the lowest when the highest-dose of As2O3 was used.There was significant difference among the PCNA indexes (PCNA L1) of the five groups. Of them, three arsenic groups all showed decrease of different degrees, and this downregulation was most obvious in group A. There was significant difference among the three groups (P=0.016).Under the light microscope, the rat kidney in the cisplatin group exhibited tubular epithelium swelling and degeneration, protein casts in collecting tubules; While all arsenic groups didn't show the significant changes (P=0.013).In the arsenic groups, the expression of bcl-2 in the renal tubular epithelium was increased (P=0.005), no obvious changes happened to PCNA L1. But in the group of cisplatin,the PCNA L1 increased significantly (P=0.001).CONCLUSION: AS2O3 can induce apoptosis of rat hepatocellular carcinoma cells. And there is optimum dose;too high dose will induce the cytotoxic effect, while certain dose of As2O3 is able to block the cell cycle at G2/M phase.As2O3 had the most remarkable influence on G2/M cells,and it can also induce apoptosis to cells at other phases.As2O3 can restrain the proliferation of rat hepatocellular carcinoma cells, in a dose-time dependent manner.Compared with cisplatin, As2O3 didn't show obvious renal toxicity, which was related to the increasing expression of bcl-2 in renal tubular epithelium, the inhibition of apoptosis and the anti-oxidation effects. | Shao-Shan Wang Ti Zhang Xi-Lu Wang Li Hong Department of Surgery of Dagang Hospital 300270,Tianjin,China Qing-Hui Qi Department of Chinese and Western Integral Surgery of Master Hospital of Tianjin Medical University 300052,Tianjin,China | 2003 | World Journal of Gastroenterology2003，9，5： | 17 |
| 6 | Differential expression of genes during aflatoxin B_1-induced hepatocarcinogenesis in tree shrews显示文摘AIM:Through exploring the regulation of gene expression during hepatocarcinogenesis induced by aflatoxin B1 (AFB1),to find out the responsible genes for hepatocellular carcinoma (HCC) and to further understand the underlying molecular mechanism.METHODS:Tree shrews ( Tupaia belangeri chinensis)were treated with or without AFB1 for about 90 weeks. Liver biopsies were performed regularly during the animal experiment. Eight shares of total RNA were respectively isolated from 2 HCC tissues, 2 HCC-surrounding noncancerous liver tissues, 2 biopsied tissues at the early stage(30^th week) of the experiment from the same animals as above, 1 mixed sample of three liver tissues biopsied at the beginning (0^th week) of the experiment, and another i mixed sample of two liver tissues from the untreated control animals biopsied at the 90^th week of the experiment. The samples were then tested with the method of Atlas^TM cDNA microarray assay. The levels of gene expression in these tissues taken at different time points during hepatocarcinogenesis were compared.RESULTS:The profiles of differently expressed genes were quite different in different ways of comparison.At the same period of hepatocarcinogenesis, the genes in the same function group usually had the same tendency for up-or down-regulation. Among the checked 588 genes that were known to be related to human cancer, 89 genes (15.1%) were recognized as “important genes” because they showed frequent changes in different ways of comparison. The differentially expressed genes during hepatocarcinogenesis could be classified into four categories: genes up-regulated in HCC tissue, genes with similar expressing levels in both HCC and HCC-surrounding liver tissues which were higher than that in the tissues prior to the development of HCC,genes down-regulated in HCC tissue, and genes up-regulated prior to the development of HCC but down-regulated after the development of HCC.CONCLUSION: A considerable number of genes could change their expressing levels both in HCC and in HCC-surrounding non-cancerous liver tissues. A few modular genes were up-regulated only in HCC but not in surrounding liver tissues, while some apoptosis-related genes were down-regulated in HCC and up-regulated in surrounding liver tissues. To compare gene-expressing levels among the liver tissues taken at different time points during hepatocarcinogenesis may be helpful to locate the responsible gene (s) and understand the mechanism for AFB1 induced liver cancer. | YuanLi Da-FangWan Jian-JiaSu Jicao ChaoOu Xiao-KunQiu Ke-ChenBan ChunYang Liu-LiangQin DanLuo Hui-FenYue Li-ShengZhang Jian-RenGu | 2004 | World Journal of Gastroenterology2004，10，4： | 11 |
| 7 | Gene expression profiles of hepatoma cell line HLE显示文摘AIM: To investigate the global gene expression of cancer related genes in hepatoma cell line HLE using Atlas Human Cancer Array membranes with 588 well-characterized human genes related with cancer and tumor biology.METHODS: Hybridization of cDNA blotting membrane was performed with 32P-labeled cDNA probes synthesized from RNA isolated from Human hepatoma cell line HLE and noncirrhotic normal liver which was liver transplantation donor.AtlasImage, a software specific to array, was used to analyze the result. The expression pattern of some genes identified by Atlas arrays hybridization was confirmed by reverse transcription polymerase chain reaction (RT-PCR)in 24 pairs of specimens and Northern blot of 4 pairs of specimens.RESULTS: The differential expression of cell cycle/growth regulator in hepatocellular carcinoma (HCC) showed a stronger tendency toward cell proliferation with more than 1.5-fold up-regulation of Cyclin C, ERK5, ERK6, E2F-3, TFDP2 and CK4. The anti-apoptotic factors such as Akt-1 were up-regulated, whereas the promotive genes of apoptosis such as ABL2 were down-regulated. Among oncogene/tumors suppressors, SKY was down-regulated. Some genes such as Integrin beta 8, Integrin beta 7, DNA-PK, CSPCP,byglycan, Tenacin and DNA Topo were up-regulated. A number of genes, including LAR, MEK1, eps15, TDGF1,ARHGDIA were down-regulated. In general, expression of the cancer progression genes was up-regulated, while expression of anti-cancer progression genes was downregulated. These differentially expressed genes tested with RT-PCR were in consistent with cDNA array findings.CONCLUSION: Investigation of these genes in HCC is helpful in disclosing molecular mechanism of pathogenesis and progression of HCC. For the first time few genes were discovered in HCC. Further study is required for the precise relationship between the altered genes and their correlation with the pathogenesis of HCC. | Lian-XinLiu Zhi-HuaLiu Hong-ChiJiang Wei-HuiZhang Shu-YiQi JieHu Xiu-QinWang MinWu | 2003 | World Journal of Gastroenterology2003，9，4： | 10 |
| 8 | Biological characteristics of HCC by ultrasound-guided aspiration biopsy and its clinical application显示文摘AIM: To probe the pathological biological characteristics of hepatocellular carcinoma (HCC) by the ultrasound-guided aspiration biopsy and assess the clinical application value of this method.METHODS: The biopsy and DNA analysis by flow cytometry (FCM) were taken in 46 cases with HCC nodules, including 26 cases and 20 cases with nodules ≤3 cm and >3 cm in diameters respectively, and 12 cases with intrahepatic benign hyperplastic nodules. They were taken in 22 cases of 46cases with HCC before and after the therapy. Fine-needles and automatic histological incised biopsy needles were used.The fresh biopsy tissue was produced into the single cell suspension, which was sent for DNA detection and ratio analysis of cell period. The ratio of each DNA period of cell proliferation of each group was calculated and compared with each other. The DNA aneuploid (AN) and apoptosis cell peak were observed and their percentages were calculated.RESULTS: The ratios of S and G2/M periods of DNA, which reflect cell hyperproliferation, in the group with HCC tumors >3 cm in diameter were markedly higher than those of the group with HCC nodules ≤3 cm in diameter and the group with the benign hyperplastic nodules (P<0.01 except A:B of S period, P<0.05). The ratios of the middle group were also apparently higher than those of the latter group (P<0.01).The ratio of DNA AN of 46 cases with HCC nodules was 34.8 % (16/46). None of the cases with the intrahepatic hyperplastic nodules appeared AN. The DNA AN appeared more apparently with the growth of the tumors. The AN ratio of the group with tumors >3 cm in diameter was 55 %(11/20), markedly higher than that of the group with tumors ≤3 cm in diameter which was 19.2 % (5/26) (P<0.01). The FCM DNA analysis of 22 specimens of hepatic carcinoma tissue before therapy showed that the aneuploid peaks appeared in 5 cases (22.7 %). The ratio of G1 period rose after therapy while the S period and G2/M ratios fell (P<0.01).The aneuploid peak disappeared in the 5 cases after the therapy, while the apoptosis peaks in 12 cases (54.5 %)appeared.CONCLUSION: Addition to supply the information of the pathological morphology of the tumor, the ultrasound-guided fine-needle aspiration tissue could be sent for FCM DNA analysis to comprehend its pathological biological characteristics. This can not only provide the clinic the reliable information about the occurrence, development,diagnosis, curative effect and prognosis of tumors but also supply biological information for clinic to choose therapeutic schemes. | Li-Wu Lin Xue-Ying Lin Yi-Mi He Shang-Da Gao Xiao-Dong Lin Fujian Provincial Ultrasonic Medicine Institute,Ultrasound Department,Union Hospital of Fujian Medical University,Fuzhou 350001,Fujian Province,China | 2003 | World Journal of Gastroenterology2003，9，5： | 7 |
| 9 | 药敏实验指导的区域化疗对不能手术切除肝癌的治疗作用显示文摘目的探讨区域灌注依据药敏实验选择的化疗药物对不能手术切除的肝癌患者的疗效。方法120例不能手术切除的原发性肝癌患者随机分组,实验组按药敏实验选择化疗药经肝动脉/门静脉化疗泵输入,对照组经肝动脉栓塞化疗。对比两组患者的肿瘤反应率、甲胎蛋白(AFP)变化、并发症、二期手术切除率和生存时间。结果实验组肿瘤缩小或稳定分别为28、14例,对照组为17、7例。实验组AFP下降为51例而对照组为30例(P〈0.05)。实验组中位随访21个月,6、12、18个月无进展生存率(PFS)及总生存期(OS)分别为:78%、70%、65%和86%、72%、65%,优于对照组(P〈0.05),实验组的化疗不良反应较对照组低(P〈0.01)。结论药敏指导不能手术切除的原发性肝癌区域灌注化疗可延长生存时间并降低并发症发生率。 | 吴东德 夏晓勤 刘宝珍 袁玉峰 刘志苏 | 2013 | 中华实验外科杂志2013，30，3： | 5 |
| 10 | Transcriptional gene expression profiles of HGF/SF-met signaling pathway in colorectal carcinoma显示文摘AIM: To explore the transcriptional gene expression profiles of HGF/SF-met signaling pathway in colorectal carcinoma to understand mechanisms of the signaling pathway at so gene level.METHODS: Total RNA was isolated from human colorectal carcinoma cell line LoVo treated with HGF/SF (80 ng/L)for 48 h. Fluorescent probes were prepared from RNA labeled with cy3-dUTP for the control groups and with cy5-dUTP for the HGF/SF-treated groups through reversetranscription. The probes were mixed and hybridized on the microarray at 60 ℃ for 15-20 h, then the microarray was scanned by laser scanner (GenePix 4000B). The intensity of each spot and ratios of Cy5/Cy3 were analyzed and finally the differentially expressed genes were selected by GenePix Pro 3.0 software. 6 differential expression genes (3 up-regulated genes and 3 down-regulated genes) were selected randomly and analyzed by β-actin semiquantitative RT-PCR.RESULTS: The fluorescent intensities of built-in negative control spots were less than 200, and the fluorescent intensities of positive control spots were more than 5000.Of the 4004 human genes analyzed by microarray, 129 genes (holding 3.22 % of the investigated genes) revealed differential expression in HGF/SF-treated groups compared with the control groups, of which 61 genes were up-regulated (holding 1.52 % of the investigated genes) and 68 genes were down-regulated (holding 1.70 % of the investigated genes), which supplied abundant information about target genes of HGF/SF-met signaling.CONCLUSION: HGF/SF-met signaling may up-regulate oncogenes, signal transduction genes, apoptosis-related genes, metastasis related genes, and down-regulate a number of genes. The complexity of HGF/SF-met signaling to control the gene expression is revealed as a whole by the gene chip technology. | Xue-NongLi Yan-QingDing Guo-BingLiu | 2003 | World Journal of Gastroenterology2003，9，8： | 5 |
| 11 | Laminin induces the expression of cytokeratin 19 in hepatocellular carcinoma cells growing in culture显示文摘AIM: To study the abnormal cytokeratin (CK) expression,emergence of CK19 with or without CK7, in liver parenchymal cells and the role of laminin (LN), a basement membrane protein, in this process.METHODS: Six hepatocellular carcinoma (HCC) cell lines were examined for different CKs, LN and its receptor by immunocytochemistry and Western blotting. Double immunofluorescent reaction, laser-scanning confocal microscopy and an in vitro induction procedure were used to demonstrate the role of LN in regulating CK19 expression in these cells.RESULTS: Immunoreactivities for CK8, CK18, CK7 and the receptor for LN were observed in all the six HCC cell lines examined. However, CK19 was merely found in four of the six cell lines, and was in any case associated with LN expression. Laser-scanning confocal microscopydemonstrated the concomitant presence of these two molecules in most of the positive cells. In the two HCC cell lines, originally negative for CK19, addition of LN to the culture medium resulted in an induction of CK19 in a dosedependent manner. Both the artificially induced and the intrinsic production of CK19 were completely blocked by an antibody to LN.CONCLUSION: LN can induce expression of CK19 in HCC cells in vitro, providing direct evidence for our hypothesis that the abnormal hepatocytic CK19 expression in situ is due to pathologic LN deposition. | QinSu YongFu Yan-FangLiu WeiZhang JieLiu Chun-MeiWang | 2003 | World Journal of Gastroenterology2003，9，5： | 5 |
| 12 | 整合素β1亚家族与肝癌粘附转移的相关研究进展显示文摘整合素家族是一类由一个α亚单位和一个β亚单位通过非共价键连接而成的异二聚体跨膜糖蛋白。整合素β1亚家族是整合素家族中最重要的一类。在正常肝脏中某些不表达或低表达的整合素β1亚家族,在肝癌中高表达,从而介导细胞与细胞外基质(ECM)的粘附,接受并传导级联信号以调节肝癌细胞存活、凋亡、粘附运动等,在肝癌的粘附、转移中起着重要作用。 | 郑继军 王阁 | 2005 | 中国肿瘤临床2005，32，24： | 4 |
| 13 | β_1整合素过表达抑制顺铂诱导肝癌细胞凋亡的实验研究显示文摘目的探讨β1整合素过表达对顺铂诱导肝癌细胞凋亡的影响及其机制。方法功能性β1整合素稳定过表达Hep3B细胞系用于实验。采用WST-1细胞增殖实验试剂盒检测细胞增殖,DNA梯形条带和Hoechst33342荧光染色检测细胞凋亡。结果与亲株、空载体转染Hep3B细胞相比,β1整合素过表达明显抑制顺铂诱导的肝癌细胞凋亡。细胞外信号调节激酶(ERK)抑制物PD98059和p38促分裂原活化蛋白激酶(MAPK)抑制物SB203580能够明显减弱β1整合素对细胞凋亡的保护作用,但Jun激酶抑制物SP600125不能减弱β1整合素的保护作用。结论β1整合素能够通过ERK和p38MAPK信号通路抵抗顺铂诱导的肝癌细胞凋亡。β1整合素介导的细胞外基质信号与肝细胞肝癌化疗耐药有关。 | 李昱骥 张浩 周建平 孔凡民 董晓申 董明 | 2008 | 中国医科大学学报2008，37，4： | 3 |
| 14 | 肝硬化及肝癌组织中整合素β1表达的差异显示文摘目的 探讨整合素β1在肝癌发生、发展中的作用.方法 应用逆转录聚合酶链反应和激光扫描共聚焦显微镜免疫荧光染色方法分别检测23份正常肝脏组织、152份肝硬化肝组织和105份肝癌组织中整合素β1 mRNA及蛋白的表达水平和分布情况,分析整合素β 1基因的表达与肝细胞肝癌临床、病理参数的关系.采用SPSS12.0统计分析软件对整合素β1表达结果及其临床病例参数的关系进行pearson x2检验,直线相关分析,pearson列联相关分析,单因素方差分析.结果 (1)整合素β1 mRNA及蛋白的相对表达量在肝癌组织分别为1.30±0.24和90.50±33.50、肝硬化组织分别为1.58±0.31和123.10±38.90、正常肝组织分别为0.37±0.08和11.90±6.00,肝癌组织、肝硬化组织中整合素β 1 mRNA及蛋白的表达均明显高于正常肝组织,F值分别为9.584和7.633,P<0.01,差异有统计学意义.(2)肝组织整合素β 1 mRNA及蛋白表达量与肝纤维化半定量评分呈正相关(mRNA:r=0.546,P<0.05;蛋白:r=0.692,P<0.01),而与肝功能无明显相关性.整合素β1的表达与肝癌Edmondson病理分级、有无包膜侵犯、有无转移、HBsAg感染呈正相关,而与肿瘤大小、结节数目、甲胎蛋白水平无明显相关性. 结论整合素素β1可能参与了肝纤维化--肝硬化--肝癌这一动态的病理过程,在肝细胞恶性转化中发挥重要作用. | 赵刚 崔静 钦琦 黎少山 殷涛 陈立波 吴河水 王春友 | 2010 | 中华肝脏病杂志2010，18，5： | 3 |
| 15 | 膜联蛋白Ⅱ在胃癌组织中的表达及其在胃癌转移中的作用显示文摘目的探讨膜联蛋白Ⅱ(AnnexinⅡ)在胃癌组织中的表达及其在胃癌转移中的作用。方法采用免疫组织化学法检测AnnexinⅡ在51例胃癌组织和24例癌旁组织中的表达,并统计AnnexinⅡ阳性表达与胃癌患者临床特征的关系。用AnnexinⅡ特异性si RNA在胃癌HGC-27细胞抑制AnnexinⅡ的表达,应用黏附实验、侵袭实验检测抑制AnnexinⅡ表达后对胃癌细胞的黏附、侵袭能力的影响。结果 AnnexinⅡ蛋白在胃癌组织中阳性率为82.4%,在癌旁组织中阳性率为37.5%,两组比较差异有统计学意义(P﹤0.01);并且AnnexinⅡ阳性表达与患者的性别与年龄无关(P﹥0.05),而与肿瘤大小、组织分化程度、临床分期、淋巴结转移临床特征有关,差异具有统计学意义(P﹤0.05)。在胃癌HGC-27细胞转染AnnexinⅡsi RNA后,细胞中AnnexinⅡ的蛋白和m RNA水平均下降,差异有统计学意义(P﹤0.05)。并且抑制AnnexinⅡ表达后,胃癌HGC-27细胞的黏附、侵袭能力下降,差异有统计学意义(P﹤0.05)。结论 AnnexinⅡ在胃癌组织中高表达,AnnexinⅡ蛋白表达与肿瘤大小、组织分化程度、临床分期、淋巴结转移临床特征有关,并且AnnexinⅡ高表达可促进胃癌转移。因此,AnnexinⅡ可以作为抑制胃癌转移的潜在靶点,开发靶向AnnexinⅡ的药物可能成为治疗胃癌转移的新方法。 | 韩峰 黄华 吕黄勇 聂川 林玲 | 2016 | 癌症进展2016，14，7： | 3 |
| 16 | Talin及Integrin/FAK信号通路与肝癌显示文摘肿瘤细胞黏附能力的改变是肿瘤细胞侵袭和转移的起始;整合素(integrin)是细胞表面重要的黏附分子受体,介导许多信号通路的发生,包括Integrin/黏着斑激酶(focal adhesion kinase,FAK)信号通路,直接或间接地影响肿瘤复发和转移,其中Integrin/FAK信号转导通路,在Integrin介导的肝癌黏附转移信号转导通路中起着至关重要的作用.踝蛋白(Talin)是第一个被证实的Integrin活化蛋白,是黏着斑(focal adhesion plaque,FAP)结构的重要组成部分.本文就Talin结构、功能、与Integrin/FAK信号通路的相互作用及其与肝癌及其他肿瘤的关系作一综述. | 张剑林 钱叶本 | 2010 | 国际外科学杂志2010，37，6： | 2 |
| 17 | 整合素α6β_1与肝癌侵袭转移的关系显示文摘 | 王旦 陈向荣 吴建胜 | 2005 | 实用医学杂志2005，21，16： | 2 |
| 18 | 热休克蛋白70与IL-2对小鼠肝癌移植模型的治疗比较显示文摘目的:比较分析肿瘤热休克蛋白70(HSP70)与IL-2对小鼠肝癌移植模型的治疗作用,评价HSP70的疗效,为应用HSP70治疗人类恶性肿瘤提供有重要参考价值的实验依据。方法:细胞培养、蛋白质纯化技术、电泳技术、Westernblot法、动物实验等。结果:IL-2及HSP70对小鼠肝癌移植模型均有治疗作用,其中IL-210万U、HSP7010μg效果最佳,IL-25万U及HSP705μg有部分治疗作用,10万U的IL-2与5μgHSP70治疗效果相当,HSP7010μg治疗后有40%小鼠移植肿瘤全部消退,长期生存790d,与对照组及其他各组相比,差异具有显著性(P<0.01,P<0.05)。结论:HSP70具有良好的抗肿瘤免疫活性,其疗效明显优于IL-2,本研究对于应用HSP70治疗人类的恶性肿瘤有十分重要的借鉴意义。 | 傅庆国 沈晓东 孟凡东 郭仁宣 | 2003 | 世界华人消化杂志2003，11，4： | 2 |
| 19 | 肝细胞肝癌组织中整合素仪α_6及β_1 mRNA的表达研究显示文摘原发性肝细胞肝癌(HCC)的预后远较其他癌症者,早期侵袭转移是重要因素之一,导致其5生存率极低。在肿瘤侵袭进程中,必须成功地完成3个过程:黏附细胞外基质(ECM)的蛋白质, | 王旦 黄智铭 黄磊 吴建胜 陈向荣 徐昌隆 陈民新 韩清锡 | 2006 | 中华内科杂志2006，45，7： | 2 |
| 20 | Integrin β1表达与肝癌组织硬化程度及病理特征相关研究显示文摘目的检测整合素β1在肝癌组织中不同部位的表达,探讨整合素β1与肝癌发生、浸润、转移和复发的关系。方法应用RT—PCR和激光扫描共聚焦显微镜免疫荧光染色方法分别检测71例肝癌病人的肝癌、癌旁和肝癌远处肝组织中整合素β1mRNA及蛋白的表达水平和分布情况,分析整合素β1基因的表达与肝癌临床、病理参数的关系。结果(1)癌旁、肝癌远处肝组织中整合素β1mRNA及蛋白的表达与肝纤维化硬化程度呈正相关;(2)整合素plmRNA及蛋白的表达与肝癌病理分级,包膜侵犯,远处转移,HBsAg感染呈正相关。结论整合素β1可能参与肝纤维化-肝硬化-肝癌这一动态的病理过程改变,与肝癌的发生、侵袭和转移有关。 | 崔静 赵刚 黎少山 钦琦 吴河水 王春友 | 2009 | 中华肝胆外科杂志2009，15，12： | 1 |
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