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| 1 | Immunohistochemical analysis of p53,cyclinD1,RB1,c-fos and N-ras gene expression in hepatocellular carcinoma in Iran显示文摘AIM: To study the effect of some genes especially those involved in cell cycle regulation on hepatocellular carcinoma. METHODS: Paraffin-embedded tissue samples of 25 patients (18 males and 7 females) with hepatocellular carcinoma were collected from 22 pathology centers in Tehran during 2000-2001, and stained using immunohistochemistry method (avidin-biotin-peroxidase) for detection of p53, cyclinD1, RB1, c-fos and N-ras proteins. RESULTS: Six (24%), 5 (20%), 12 (48%) and 2 samples (8%) were positive for p53, cyclinD1, C-fos and N-ras expression, respectively. Twenty-two (88%) samples had alterations in the G1 cell-cycle checkpoint protein expression (RB1 or cyclinD1). P53 positive samples showed a higher (9 times) risk of being positive for RB1 protein than p53 negative samples. Loss of expression of RB1 in association with p53 over-expression was observed in 4 (66.7%) of 6 samples. Loss of expression of RB1 was seen in all cyclinD1 positive, 20 (90.9%) N-ras negative, and 11 (50%) C-fos positive samples, respectively. CyclinD1 positive samples showed a higher (2.85 and 4.75 times) risk of being positive for c-fos and N-ras expression than cyclinD1 negative samples. CONCLUSION: The expression of p53, RB1 and c-fos genes appears to have a key role in the pathogenesis of hepatocellular carcinoma in Iran. Simultaneous overexpression of these genes is significantly associated with their loss of expression during development of hepatocellular carcinoma. | SJ Moghaddam EN Haghighi S Samiee N Shahid AR Keramati S Dadgar MR Zali | 2007 | World Journal of Gastroenterology2007，13，4： | 73 |
| 2 | Constitutive activation of Stat3 signaling pathway in human colorectal carcinoma显示文摘AIM: Signal transducers and activators of transcription (STATs) are a family of transcription factors activated in response to cytokines and growth factors. Constitutive activation of Stat3 has been observed in a growing number of tumor-derived cell lines, as well as tumor specimens from human cancers. The purpose of this study was to investigate the expression of p-Stat3, activated form of Stat3, and its downstream mediators including cyclin D1 and Bcl-XL in colorectal carcinoma (CRC), and to explore the possible mechanism of Stat3 signaling pathway in the tumorigenesis of colorectal carcinoma. METHODS: Tissue samples from 45 patients of primary colorectal carcinoma were selected for studying Stat3 signaling pathway protein expression. Western blot analysis was used to measure the expression of p-Stat3, cyclin D1, and Bcl-xu proteins in colorectal carcinomas. Furthermore, the expression patterns of these proteins were analyzed for their distribution at the cellular level by immunohistochemical staining of the tissues. RESULTS: Protein levels of p-Stat3, cyclin D1, and Bcl-XL were increased in colorectal carcinomas compared with adjacent normal mucosae (P<0.05). Elevated levels of pStat3 were correlated with the nodal metastasis and the stage (P<0.05). Overexpression of cyclin D1 was associated with the nodal metastasis (P<0.05). There was also a significant correlation between the expressions of p-Stat3 and cyclin D1 (r=0.382, P<0.05). CONCLUSION: Constitutive activation of Stat3 may play an important role in the tumorigenesis of colorectal carcinoma, and the detailed mechanism of Stat3 signaling pathway in CRC deserves further investigation. | Xiang-TaoMa ShanWang Ying-JiangYe Ru-YuDu Zhi-RongCui MaSomsouk | 2004 | World Journal of Gastroenterology2004，10，11： | 68 |
| 3 | The promoting molecular mechanism of alphafetoprotein on the growth of human hepatoma Bel7402 cell line显示文摘AIM: The goal of this study was to characterize the AlPreceptor, its possible signal transduction pathway and itsproliferative functions in human hepatoma cell line Bel 7402.METHODS: Cell proliferation enhanced by AFlP was detectedby MTT assay, 3H-thymidine incorporation and S-stsgepercentage of cell cycle analysis. With radioactive labeled 125 I-AFP for receptor binding assay; cAMP acctmuation, ProteinKinase A activity were detected by radioactive immunosorbentassay and the change of intracellular free calcium ([Ca2+ ], )was monitored by scanning fluorescence intensity under TCS-NT confocal microscope. The expression of oncxgenes N- ras,p53, and p21ras in the cultured cells in vitro were detected byNorthem blotting and Western blotting respectively.RESULTS: It was demonstrated that AFP enhanced theproliferation of human hepatoma Bel 7402 cell in a dosedependlent fashion asshown in MTT assay, 3H-thymidineincorporation and S-phase percentage up to 2-fold. Twosubtypes of AFP receptors were identified in the cells withKds of 1.3 x 10-9 mol. L-1 and 9.9 x 10-8 mol. L-1 respectively.Pretreatnent of cells with AFP resulted-in a significantincrease (625 %) in cAMP accumulation. The activity ofprotein kinase A activity were increased up to 37.5, 122.6,73.7 and 61.2 % at treatment time point 2, 6, 12 and 24hours. The level of intracellular calcium were elevated afterthe treatment of alpha-fetoprotsin and achieved to 204 % at 4min. The results also showed that AFP (20 mg. L-1 ) couldupregulate the expression of N-ras oncogenes and p53 andp21ras in Bel 7402 cells. In the later case, the alteration ware 81.1%(12 h) and 97.3 %(12 h) respectively compared with control.CONCLUSION: These results demonstrate that AFP is apotential growth factor to promote the proliferation of humanhepatoma Bel 7402 cells. Its growth-regulatory effects aremediated by its specific plasma membrane receptorscoupled with its transmembrane signaling transductionthrough the pathway of cAMP-PKA and intracellular calciumto regulate the expression of oncogenes. | LiMS LiPF 等 | 2002 | World Journal of Gastroenterology2002，8，3： | 59 |
| 4 | Seek protein which can interact with hepatitis B virus X protein from human liver cDNA library by yeast two-hybrid system显示文摘AIM: To seek the X associated protein (XAP) with theconstructed bait vector pAS2-1X from normal human livercDNA library.METHODS: The X region of the HBV gene was amplied byPCR and cloned into the eukaryotic expression vector pAS2-l.The reconstituted plasmid pAS2-1X was transformed intothe yeast cells and the expression of X protein (pX) wasconfirmed by Western blot analysis. Yeast cells werecotransformed with pAS2-1X and the normal human livercDNA library and were grown in selective SC/-trp-leu-his-ade medium, the second screen was performed with theLacZ report gene. Furthermore, segregation analysis andmating experiment were performed to eliminate the falsepositive and the true positive clones were selected for PCRand sequencing.RESULTS: Reconstituted plasmid pAS2-1X including theanticipated fragment of X gene was proved by auto-sequencing assay. Western blot analysis showed thatreconstituted plasmid pAS2-1X expressed BD: X fusionprotein in yeast cells. Of 5 × 106 transformed coloniesscreened, 65 grew in the selective SC/-trp-leu-his-ademedium, 5 scored positive for β-gal activity, and only 2remaining clones passed through the segregation analysisand mating experiment. Sequence analysis identified thattwo clones contained similar cDNA fragment: GAACFFGCG.CONCLUSION: The short peptide (glutacid-leucine-alanine)is a possible required site for XAP binding to pX. Normalhuman liver cDNA library has difficulties in expressing theintegrated XAP on yeast cells. | Xian-ZhongWang Xiang-RongJiang 等 | 2002 | World Journal of Gastroenterology2002，8，1： | 46 |
| 5 | Inhibitory effect of octreotide on gastric cancer growth via MAPK pathway显示文摘AIM: Somatostatin and its analogues may suppress the growth of various tumor cells. However, the effect of octreotide on growth of gastric adenocarcinoma is still largely unknown. This study was to explore if octreotide could inhibit the growth of gastric adenocarcinoma and its probable mechanisms.METHODS: Proliferation of gastric cancer cell line affected by octreotide was determined by 3H-thymidine incorporation.After xenografts of human gastric cancer were implanted orthotopically in stomach, nude mice were administrated octreotide for 8 weeks. The mRNA of somatostatin receptor in the SGC-7901 cells was detected by reverse transcription polymerase chain reaction technique. Extracellular signalregulated protein kinase and c-Fos in gastric cancer tissues were measured by immunohistochemistry and Western blot.Activator protein-1 binding activity was examined by electrophoretic mobility sift assay.RESULTS: 3H-thymidine incorporation into SGC-7901 cells was significantly decreased by octreotide in a concentration dependent manner. Either size or weight of tumors treated with octreotide was significantly reduced in vivo. The inhibition rate for tumor was 62.3% in octreotide group.The genes of somatostatin receptors 2 and 3 were expressed in SGC-7901 gastric cancer cell lines. Extracellular signal-regulated protein kinase and c-Fos protein level were decreased in gastric adenocarcinoma treated with octreotide. Moreover, fetal calf serum stimulated activator protein-1 binding activity could be suppressed by octreotide potentially.CONCLUSION: Inhibition of sequential molecular events in MAPK pathway may interpret the mechanisms underlying the effect of octreotide on the growth of gastric adenocarcinoma. | Chun-HuiWang Cheng-WeiTang Chun-LunLiu Li-PingTang | 2003 | World Journal of Gastroenterology2003，9，9： | 33 |
| 6 | Expression of p53 and C-myc genes and its clinical relevance in the hepatocellular carcinomatous and pericarcinomatous tissues显示文摘AIM: To investigate the possible roles of p53 and C-mycgenes in the primary hepatocellular carcinogenesis and therelationship between the liver hyperplastic nodule(LHN) andhepatocellular carcinoma(HCC).METHODS: The expression of p53 and C-myc genes wasdetected immunohist-ochemically in 73 and 60 cases of HCCand pericarcinomatous tissues, respectively .RESULTS: The positive expression of p53 in HCC wassignificantly higher than that in pericarcinomatous tissues(P<0.05). In pericarcinomatous tissues, the p53 expressionwas observed only in LHN, but not in liver cirrhosis (LC) andnormal liver tissues. The positive expression rate of C-mycin HCC or LHN was significantly higher than that in LC ornormal liver tissues (P<0.05 and P<0.01), however, nosignificant difference was found between HCC and LHN(P>0.05). The positive expression rate of p53 and C-myc inHCC was correlated with the histological differentiation, thatin the poorly differentiated was significantly higher than thatin well differentiated samples (P<0.05).CONCLUSION: The overexpression of p53 and C-myc genesmight play a role in the carcinogenesis of HCC; And LHNseems a preneoplastic lesion related to hepatocarcinogenesis;No evidence supports that LC contribute directly to thehepatocarcinogenesis. | Zhao-Shan Niu Bo-Kian Li Department of Pathology,Medical College of Qingdao University,Qingdao 266021,Shandong Province,China Mei Wang Department of Foreign languages,Qingdao institute of Architecture and Engineering,Qingdao 266033,Shandong Province,China | 2002 | World Journal of Gastroenterology2002，8，5： | 30 |
| 7 | p38MAPK在大鼠实验性肝纤维化发生中的表达及其意义显示文摘目的:观察p38MAPK在实验性大鼠肝纤维化(hepatic fibrosis,HF)发生过程中表达量的变化及其定位,从而揭示p38MAPK信号传导通路与HF形成之间的关系.方法:采用CCl4sc诱导大鼠HF模型,36只♂SD大鼠(体质量在180-220g)随机分为正常对照组(12只)和CCl4造模组(24只),造模3、6、9wk结束时分别随机处死各组大鼠.取其肝脏观察HF形成过程中不同时间段各组大鼠肝组织病理变化,用RT-PCR技术检测p38MAPK mRNA在造模过程中肝组织中的表达变化,免疫组化方法检测p38MAPK在造模过程中肝组织中蛋白表达量的变化,及其在肝组织中的表达分布情况.结果:与正常对照组比较,CCl4诱导的实验性大鼠HF不同时间段纤维化程度明显加重,随着HF的形成,p38MAPK在mRNA水平和蛋白水平都表现出增加的趋势,并且主要表达于肝脏的间质细胞,肝细胞未见染色.结论:p38MAPK在HF的形成中持续上调,参与HF形成的病理过程,p38MAPK信号传导通路活化可能促进CCl4诱导的HF的形成. | 吴文娟 杨妙芳 许小兵 张晓华 季洪赞 袁柏思 朱人敏 | 2008 | 世界华人消化杂志2008，16，34： | 22 |
| 8 | Activation of JNK by TPA promotes apoptosis via PKC pathway in gastric cancer cells显示文摘AIM: JNK cascade plays an important role in cell proliferation, differentiation and apoptosis. However, the exact function of JNK cascade for apoptosis induction remains largely unknown. In this study, the role of JNK activation stimulated by TPA in the process of apoptosis induction and its signaling transduction pathway in gastric cancer cells were investigated and determined.METHODS: Expressions of mRNA and protein were detected by Northern blot and Western blot. Transcription activity was measured by transient transfection and CAT assay. Apoptotic cells were displayed through staining the nucleus with DAPI and were observed under fluorescence microscope. The apoptotic index was determined by counting 1000 cells randomly.RESULTS: JNK protein was stimulated rapidly by TPA, and reached its highest peak within 3 hr, then decreased in a time-dependent manner, but the expression level of JNK protein induced by TPA was always keeping higher than that in untreated cells. Similar pattern was seen in c-jun mRNA level induced by TPA. TPA significantly activated the transcriptional activity of activator protein-1 with a TPA-closedependent manner. Furthermore, activation of JNK was mediated through PKC pathway. Treatment of cells with PKC specific inhibitor, Wortmannin, led to repression of JNK even in the presence of TPA. More importantly, all these effects were associated with induction of apoptosis in gastric cancer cells. TPA inducted apoptosis obviously in gastric cancer cells. The apoptotic cells became smaller and rounded, and their nuclei became condensation and fragmentation with brightly stained chromatin. However, suppression of JNK by PKC specific inhibitor, Wortmannin, resulted in the decrease of apoptosis induced by TPA in a time-dependent manner, apoptotic index dramatically decreased from 32.56 % to 8.71%.CONCLUSION: TPA stimulates JNK cascade, including upregulation of JNK protein expression level and c-jun mRNA expression level, and activation of activator protein-1 transcriptional activity. Activation of JNK is mediated through PKC pathway, which has an association with induction of apoptosis by TPA. Thus, activation of JNK via PKC pathway may represent one of important mechanisms for TPA to induce apoptosis in gastric cancer cells. | Yan Chen Qiao Wu Si-Yang Song Wen-Jin Su,Key Laboratory of the Ministry of Education for Cell Biology and Tumor Cell Engineering,The School of Life Sciences,Xiamen University,Xiamen,Fujian Province,361005,China | 2002 | World Journal of Gastroenterology2002，8，6： | 18 |
| 9 | Antiproliferative and proapoptotic effects of somatostatin on activated hepatic stellate cells显示文摘AIM: To assess the effects of somatostatin on proliferation and apoptosis of activated rat hepatic stellate cells (HSCs). METHODS: HSCs isolated from the livers of adult SpragueDawley rats (weighing 400-500 g) by in situ perfusion and purified by single-step density gradient centrifugation with Nycodenz, became activated after 10 days' cultivation. Then the apoptotic rate of HSCs treated with different doses of somatostatin for 72 h, was assayed by acridine orange/ethidium bromide fluorescent staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, transmission electron microscopy and flow cytometry, while the proliferation of HSCs was measured by MTT assay. Furthermore, the mechanisms of somatostatin were investigated by cytodynamic analysis. RESULTS: Somatostatin at the concentration of 10^-6-10^-99 mol/L could decrease the proliferative rate, and promote the apoptosis of activated rat HSCs in a dose-dependent way. Its action was most significant when the concentration reached 10^-6 mol/L or 10^-7 mol/L (P<0.05-0.01). An obvious cell-cycle arrest (G0/G1 arrest) was the important way for somatostatin to exert its action. CONCLUSION: Antiproliferative and proapoptotic effects of low-dose somatostatin on activated rat HSCs can be obtained. These findings reveal its potential antifibrotic action. | QinPan Ding-GuoLi Han-MingLu Liang-YongLu Yu-Qinwang Qin-FangXu | 2004 | World Journal of Gastroenterology2004，10，7： | 17 |
| 10 | Expression of Egr-1,c-fos and cyclin D1 in esophageal cancer and its precursors:An immunohistochernical and in situ hybridization study显示文摘AIM:To examine the expression of Egr-1, c-fos and cyclin D1 at both transcript and protein levels in esophageal carcinoma and to correlate the level of their expressions with precancerous and paracancerous esophageal lesions and esophageal carcinoma.METHODS:In situ hybridization and immunohistochemistry were used respectively to detect the expression of mRNA and proteins of Egr-1, c-fos and cyclin D1 in 70 cases of esophageal squamous cell carcinoma and their corresponding para-cancerous mucosa and upper cut edge mucosa.RESULTS:In situ hybridization and immunohistochemistry showed positive staining of all three mRNAs in the cytoplasm and those of the proteins in nuclei. Overexpression of Egr-1, c-los and cyclin D1 mRNAs and their proteins was found in dysplasia and squamous carcinomas. The expression level of Egr-1 and c-los was high, and cyclin D1 was low in dysplasia mucosa, whereas the expression of Egr-1 was decreased, c-fos was maintained and cyclin D1 was increased in the cancers. The expression of both c-fos and cyclinD1 was consistent between the mRNA and protein in their corresponding high expression lesions.CONCLUSION: The expression of Egr-1, c-fos and cyclin D1 varies in esophageal precancerous lesions and cancer tissues, suggesting an involvement of these genes in the development of esophageal carcinoma. | Ming-YaoWu Chu-XiangZhuang Huan-XingYang Ying-RuiLiang | 2004 | World Journal of Gastroenterology2004，10，4： | 16 |
| 11 | TECA hybrid artificial liver support system in treatment of acute liver failure显示文摘AIM: To assess the efficacy and safety of TECA type hybrid artificial liver support system (TECA-HALSS) in providing liver function of detoxification, metabolism and physiology by treating the patients with acute liver failure (ALF).METHODS: The porcine liver cells (1 - 2 ) x 1010 were separated from the Chinese small swine and cultured in the bioreactor of TECA-BALSS at 37.0°C and circulated through the outer space of the hollow fiber tubes in BALSS. The six liver failure patients with various degree of hepatic coma were treated by TECA-HALSS and with conventional medicines. The venous plasma of the patients was separated by a plasma separator and treated by charcoal adsorbent or plasma exchange. The plasma circulated through the inner space of the hollow fiber tubes of BALSS and mixed with the patients' blood cells and flew back to their blood circulation. Some small molecular weight substances were exchanged between theplasma and porcine liver cells. Each treatment lasted 6.0-7.0 h.Physiological and biochemical parameters were measured before, during and after the treatment.RESULTS: The average of porcine liver cells was (1.0- 3.0)x 1010 obtained from each swine liver using our modified enzymatic digestion method. The survival rate of the cells was 85% - 93% by tnypan blue stain and AO/PI fluorescent stain. After cultured in TECA-BALSS bioreactor for 6 h, the survival rate of cells still remained 70% - 85%. At the end of TECA-HALSS treatment, the levels of plasma NH3, ALT, TB and DB were significantly decreased. The patients who were in the state of drowsiness or coma before the treatment improved their appetite significantly and regained consciousness, some patients resumed light physical work on a short period after the treatment. One to two days after the treatment, the ratio of PTA increased warkedly. During the treatment, the heart rates, blood pressure, respiration condition and serum electrolytes (K+, Na+ and Cl) were stable without thrombosis and bleeding in all the six patients.CONCLUSION: TECA-HALSS treatment could be a rapid,safe and efficacious method to provide temporary liver support for patients with ALF. | Yi-Long Xue~1 Shi-Feng Zhao~1 Yun-Luo~1 Xin-Jian Li~1 Zhong-Ping Duan~2 Xiao-Ping Chen~1 Wen-Ge Li~1 Xiao-Qiang Huang~1 Yan-Ling Li~1 Xin-Cui~1 Da-Guang Zhong~1 Zuo-Yun Zhang~1 Zhi-Qiang Huang~1 1 Chinese PLA General Hospital,Beijing 100853,China2 Beijing You-An Hospital,Beijing 100054,China | 2001 | World Journal of Gastroenterology2001，7，6： | 15 |
| 12 | 柴胡皂甙d对人肝癌细胞STAT3/COX-2信号通路的调节作用显示文摘目的观察柴胡皂甙d(saikosaponin-d,SSd)对人肝癌细胞STAT3、COX-2表达的影响,探讨其抗肿瘤作用可能的信号通路机制。方法体外培养人肝癌SMMC-7721细胞,分别经IL-6、AG490和SSd作用后,免疫细胞化学及免疫印迹方法检测STAT3、磷酸化STAT3(p-STAT3)以及COX-2蛋白表达的变化,并探讨其关系。结果免疫细胞化学结果显示,IL-6诱导组人肝癌细胞p-STAT3和COX-2蛋白的表达较空白对照组显著升高,而加入AG490或SSd后p-STAT3、COX-2蛋白表达较IL-6诱导组明显减弱,SSd对STAT3蛋白表达则无明显影响;免疫印迹结果亦显示出类似变化:经IL-6作用,人肝癌细胞p-STAT3和COX-2的表达明显增强,AG490或SSd作用的人肝癌细胞p-STAT3表达呈现剂量依赖性下降,COX-2蛋白表达亦出现相应下调。结论p-STAT3参与了人肝癌细胞COX-2表达调节,SSd可能通过抑制STAT3磷酸化下调COX-2的表达而发挥抗肿瘤作用。 | 朱占芳 和水祥 侯和磊 卢新兰 胡雅楠 陈静宏 王治沦 | 2010 | 第三军医大学学报2010，32，18： | 15 |
| 13 | 大鼠肝纤维化中细胞外信号调节激酶的作用显示文摘目的:通过研究大鼠肝纤维化模型肝组织中细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)的表达和分布规律,初步探讨ERK信号传导通路在肝纤维化发病机制中的作用。方法:♂SD大鼠32只,质量250-300g,皮下注射CCl_4制备大鼠肝纤维化模型,分别于注射CCl_4后1,4,8wk处理动物,采用免疫组织化学方法检测肝组织中ERK1的表达及分布。结果:ERK1主要表达于肝星状细胞中。CCl_4注射诱导后,大鼠肝组织中ERK1的表达较正常对照明显增强(P<0.05),且CCl_4注射1,4,8wk组肝组织中ERK1的表达强度呈明显的逐级递增的趋势(P<0.05)。结论:ERK信号传导通路的激活促进肝星状细胞的活化增生,可能与大鼠肝纤维化的发生发展有关。 | 梁增文 张国 王天才 | 2003 | 世界华人消化杂志2003，11，6： | 15 |
| 14 | 萎胃消对萎缩性胃炎癌前病变患者PTEN和ERK_2蛋白表达的影响显示文摘目的:观察萎胃消对慢性萎缩性胃炎伴胃黏膜上皮异型增生或/和不完全型结肠上皮化生的治疗效果及PTEN和ERK2蛋白表达的影响。方法:60例患者随机分为治疗组和对照组。治疗组给予萎胃消颗粒,对照组给予维酶素,疗程3个月。观察临床症状和体征、胃镜和病理组织学变化及PTEN和ERK2的表达。结果:治疗前后症状缓解总有效率:治疗组90.00%,对照组55.67%;胃镜和病理改变总有效率:治疗组70%,对照组33.33%;2组间比较差异均有显著性(P<0.01)。PTEN和ERK2表达:治疗组治疗前后PTEN和ERK2表达差异有统计学意义(P<0.01或P<0.05),而对照组治疗前后PTEN和ERK2表达水平变化不明显。结论:萎胃消具有良好的胃癌前病变逆转治疗效应,其上调抑癌基因蛋白PTEN的表达和有效抑制ERK信号通路的异常激活可能是萎胃消治疗萎缩性胃炎癌前病变的部分作用机理。 | 钟毅 赵自明 饶梅冰 戈焰 范明 | 2012 | 中国中医基础医学杂志2012，18，2： | 12 |
| 15 | DADS诱导人胃癌细胞分化作用中ERK/AP-1通路的改变显示文摘目的 探讨ERK/AP 1通路在二烯丙基二硫 (DADS)诱导人胃癌细胞分化中的作用 ,阐明DADS诱导人胃癌细胞分化的分子机制。方法 采用免疫细胞化学、图像分析及WesternBlot等方法 ,观察DADS作用于体外培养的人胃癌MGC80 3细胞前后AP 1成员c fos与c jun表达的改变以及ERKMAPK激酶的变化。结果 免疫细胞化学及图像分析结果显示 ,对照组c fos、c jun表达呈强阳性 ,而处理组呈阴性或弱阳性 ,阳性率明显降低 ,处理组光密度值较对照组明显低 (P <0 0 5 )。WesternBlot结果显示 :从 2 0、2 5、30到 35mg·L-1DADS处理癌细胞 ,DADS呈浓度依赖性抑制人胃癌细胞中ERK的活化 (P <0 0 5 ) ;并且DADS +MEK抑制剂PD980 5 9能完全阻断ERK活化 (P <0 0 5 ) ;时间效应上 ,在DADS刺激后 15~ 30min抑制作用最强 ,2h左右恢复至接近正常 (P <0 0 5 )。结论 ERK/AP | 凌晖 宋颖 曾铁兵 袁静萍 苏琦 | 2003 | 中国药理学通报2003，19，11： | 11 |
| 16 | Inhibition of conjugated linoleic acid on mouse forestomach neoplasia induced by benzo(a)pyrene and chemopreventive mechanisms显示文摘AIM: To explore the inhibition of conjugated linoleic acidisomers in different purity (75 % purity c9,t11-, 98 % purityc9,t11- and 98 % purity t10,c12-CLA) on the formation offorestomach neoplasm and cheopreventive mechanisms.METHODS: Forestomach neoplasm model induced by B(a)P in KunMing mice was established. The numbers of tumorand diameter of each tumor in forestomach were counted;the mice plasma malondialdehyde (MDA) were measuredby TBARS assay; TUNEL assay was used to analyze theapoptosis in forestomach neoplasia and the expression ofMEK-1, ERK-1, MKP-1 protein in forestomach neoplasm werestudied by Western Blotting assay.RESULTS: The incidence of neoplasm in B(a)P group, 75 %purity c9, t11-CLA group, 98 % purity cg,t11-CLA groupand 98 % purity t10, c12-CLA group was 100 %, 75.0 %(P>0.05), 69.2 % (P<0.05) and 53.8 % (P<0.05) respectivelyand the effect of two CLA isomers in 98 % purity onforestomach neoplasia was significant; CLA showed noinfluence on the average tumor numbers in tumor-bearingmouse, but significantly decreased the tumor size, the tumoraverage diameter of mice in 75 % purity c9,t11-CLA group,98 % purity cg,t11-CLA group and 98 % purity t10, c12-CLAgroup was 0.157±0.047 cm, 0.127±0.038 cm and 0.128±0.077 cm (P<0.05) and 0.216±0.088 cm in B(a)P group;CLA could also significantly increase the apoptosis cellnumbers by 144.00±20.31, 153.75±23.25, 157.25±15.95(P<0.05) in 75 % purity c9,t11-CLA group, 98 % purity c9,t11-CLA group and 98 % purity t10,c12-CLA group (30.88±3.72 in BP group); but there were no significant differencesbetween the effects of 75 % purity c9,t11-CLA and twoisomers in 98 % purity on tumor size and apoptotic cellnumbers; the plasma levels of MDA in were increased by75 % purity c9,t11-ClA, 98 % purity c9,t11-CLA and 98 %purity t10,c12-CLA. The 75 % purity c9,t11-CLA showedstronger inhibition; CLA could also inhibit the expression ofERK-1 protein and promote the expression of MKP-1 protein,however no influence of CLA on MEK-1 protein was observed.CONCLUSION: Two isomers in 98 % purity show strongerinhibition on carcinogenesis. However, the inhibitorymechanisms of CLA on carcinogenesis is complicated, whichmay be due to the increased mice plasmaMDA, the inducingapoptosis in tumor tissues. And the effect of CLA on theexpression of ERK-1 and MKP-1 may be one of themechanisms of the inhibition of CLA on the tumor. | Bing-QingChen Ying-BenXue jia-RenLiu Yan-MeiYang Yu-MeiZheng Xuan-LinWang Rui-HaiLiu | 2003 | World Journal of Gastroenterology2003，9，1： | 11 |
| 17 | Hepatocyte transformation and tumor development induced by hepatitis C virus NS3 c-terminal deleted protein显示文摘AIM: To study the effect of hepatitis C virus nonstructural protein 3 c-terminal deleted protein (HCV NS3-5') on hepatocyte transformation and tumor development.METHODS: QSG7701 cells were transfected with plasmid pRcHCNS3-5' (expressing HCV NS3 c-terminal deleted protein) by lipofectamine and selected in G418. The expression of HCV NS3 gene and protein was determined by PCR and immunohistochemistry respectively. Biological behavior of transfected cells was observed through cell proliferation assay, anchorage-independent growth and tumor development in nude mice. The expression of HCV NS3 and c-mycproteins in the induced tumor was evaluated by immunohistochemistry.RESULTS: HCV NS3 was strongly expressed in QSG7701 cells transfected with plasmid pRcHCNS3-5' and the positive signal was located in cytoplasm. Cell proliferation assay showed that the population doubling time in pRcHCNS3-5' transfected cells was much shorter than that in pRcCMV and nontransfected cells (24 h, 26 h, 28 h respectively). The cloning ratio of cells transfected with pRcHCNS3-5; pRcCMV and nontransfected cells was 33 %, 1.46 %, 1.11%, respectively,the former one was higher than that in the rest two groups (P<0.01). Tumor development was seen in nude mice inoculated with pRcHCNS3-5' transfected cells after 15 days.HE staining showed its feature of hepatocarcinoma, and immunohistochemistry confirmed the expressions of HCV NS3and c-mycproteins in tumor tissue. The positive control group inoculated with HepG2 also showed tumor development, while no tumor developed in the nude mice injected with pRcCMV and non-transfected cells after 40 days.CONCLUSION: 1.HCV NS3 c-terminal deleted protein has transforming and oncogenic potential. 2. Human liver cell line QSG7701 may be used as a good model to study HCV NS3 pathogenesis. | Qiong-QiongHe Rui-XueCheng YiSun De-YunFeng Zhu-ChuChen HuiZheng | 2003 | World Journal of Gastroenterology2003，9，3： | 10 |
| 18 | Expression of liver cancer associated gene HCCA3显示文摘AIM: To study and clone a novel liver cancer reisted gene,and to explore the molecular basis of liver cancer genesis.METHODS: Using mRNA differential display polymerasechain reaction (DDPCR), we investigated the difference of mRNA in human hepatocellular carcinoma (HCC) and paired surrounding liver tissues, and got a gene probe. By screening a human placenta cDNA library and genomic homologous extend, we obtained a full-length cDNA named HCCA3. We analyzed the expression of this novel gene in 42pairs of HCC and the surrounding liver tissues, and distribution in human normal tissues by means of Northern blot assay.RESULTS: A full-length cDNA of liver cancer associated gene HCCA3 has been submitted to the GeneBank nucleotide sequence databases ( Accession No. AF276707 ). The positive expression rate of this gene was 78.6% (33/42) in HCC tissues, and the clinical pathological data showed that the HCCA3 was closely associated with the invasion of tumor capsule ( P = 0.023) and adjacant small metastasis satellite nodules lesions ( P= 0.041). The HCCA3 was widely distributed in the human normal tissues, which was intensively expressed in lungs, brain and colon tissues,while lowly expressed in the liver tissues.CONCLUSION: A novel full-length cDNA was cloned and differentiated, which was highly expressed in liver cancer tissues. The high expression was closely related to the tumor invasiveness and metastasis, that may be the late heredited change in HCC genesis. | Zheng-Xu Wang~1 Gui-Fang Hu~1 Hong-Yang Wang~2 Meng-Chao Wu~2 1 Department of General Surgery,Chinese PEA General Hospital of Lanzhou Military Command,Lanzhou 730050,Gansu Province,China2 Eastern Hepatobilliary Surgical Hospital,Second Military Medical University,Shanghai 200438,China | 2001 | World Journal of Gastroenterology2001，7，6： | 9 |
| 19 | 肝纤维化大鼠肝组织中NF-κB及ERK-1mRNA的表达显示文摘目的探讨核转录因子-κB(NF-κB)及细胞外信号调节激酶(ERK)mRNA在CCl4致实验性肝纤维化大鼠肝组织中的表达及其与肝纤维化的关系。方法建立CCl4致大鼠实验性肝纤维化的模型,用免疫组化法比较正常组,模型组的α平滑肌肌动蛋白(α-SMA)的表达,用RT-PCR法比较各组肝组织NF-κB以及ERK-1mRNA的表达。结果模型组中,ERK-1及NF-κBmRNA的表达均增高。结论ERK通路介导的促增殖作用与NF-κB通路介导的促炎症反应,促进HSC的激活、增殖,在肝纤维化的发生发展中均是不可或缺的。 | 胡泰洪 蒋祥虎 蒋跃明 周敏 徐敏 朱锐 杨玲 | 2009 | 临床肝胆病杂志2009，25，1： | 7 |
| 20 | 自拟胃癌消加减治疗胃癌前病变42例临床观察显示文摘目的:探讨自拟胃癌消加减治疗胃癌前病变(PLGC)的临床疗效。方法:将124例PLGC患者随机分为治疗组和对照组各42例,治疗组予自拟胃癌消加减治疗,对照组予叶酸口服治疗。比较两组患者中医证候疗效、主要症状评分、蛋白酪氨酸磷酸酶基因(PTEN)和红细胞外信号调节激酶2(ERK2)的表达情况。结果:治疗组中医证候疗效优于对照组,差异有统计学意义(P<0.05);两组患者治疗后各主要症状均较治疗前改善(P<0.05),治疗组主要症状改善情况优于对照组,差异有统计学意义(P<0.05);治疗组治疗后PTEN表达情况增加,ERK2表达降低,差异均有统计学意义(P<0.05)。结论:自拟胃癌消加减治疗胃癌前病变,疗效确切,安全性高。 | 张江 史志勇 | 2013 | 中医药导报2013，19，12： | 7 |
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