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| 1 | 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 |
| 2 | 人参皂苷单体Rh_2抑制小鼠前胃癌系细胞增殖及其机制显示文摘目的探讨人参皂苷Rh2(G-Rh2)对小鼠前胃癌系(MFC)细胞增殖的抑制作用及其机制。方法分别对MFC正常细胞组和G-Rh2(3、10、30mg.L-1)组经MTT法检测MFC细胞活性;倒置显微镜和Hoechst33258荧光染色观察凋亡细胞形态;AnnexinV-FITC双染法分析G-Rh2对细胞凋亡率的影响;分别对MFC正常细胞组、G-Rh2(10mg.L-1)处理不同时间(30min、1、2、4h)组、SP600125(5μmol.L-1)预处理2h+G-Rh2(10mg.L-1)不同时间(30min、1、2、4h)给药组经MTT法检测MFC细胞活性;Westernblot法检测G-Rh2(10mg.L-1)处理不同时间(5、15、30、45min、1、2、4h)组p-JNK(c-JunN-terminalkinase1)激酶和p-c-jun在MFC细胞中的活性,免疫细胞化学染色法检测caspase-3阳性细胞的表达率。结果G-Rh2对无血清MFC细胞有明显细胞毒活性,呈时间和剂量依赖关系;能明显诱导细胞皱缩,核染色质固缩,核碎裂,形成大约为180~200bp或其多聚体组成的寡核苷酸片断,凋亡细胞比率上升。G-Rh2处理后4h内,p-JNK激酶和p-c-jun活性持续升高,此过程可被预处理2h的SP600125(5μmol.L-1)部分抑制。结论人参皂苷G-Rh2可诱导MFC细胞凋亡,其作用机制之一可能是通过激活JNK信号传导途径,并最终增加caspase-3的激活而完成。 | 吴歌 李红 杨世杰 | 2008 | 中国药理学通报2008，24，1： | 9 |
| 3 | Roles of PLC-γ2 and PKCα in TPA-induced apoptosis of gastric cancer cells显示文摘AIM: To investigate the roles of PLCγ2 and PKCα in TPA-induced apoptosis of gastric cancer cells.METHODS: Human gastric cancer cell line MGC80-3 was used. Protein expression levels of PLCγ2 and PKCα were detected by Western blot. Protein localization of PLCγ2 and PKCα was shown by immunofluoscence analysis under laserscanning confocal microscope. Apoptotic morphology was observed by DAPI fluorescence staining, and apoptotic index was counted among 1 000 cells randomly.RESULTS: Treatment of gastric cancer cells MGC80-3 with TPA not only up-regulated expression of PLC-γ2 protein,but also induced PLC-γ2 translocation from the cytoplasm to the nucleus. However, this process was not directly associated with apoptosis induction. Further investigation showed that PKCa translocation from the cytoplasm to the nucleus was correlated with initiation of apoptosis. To explore the inevitable linkage between PLC-γ2 and PKCα during apoptosis induction,PLC inhibitor U73122 was used to block PLC-γ2 translocation,in which neither stimulating PKCα translocation nor inducing apoptosis occurred in MGC80-3 cells. However, when U73122treated cells were exposed to TPA, not only PLC-γ2, but also PKCα was redistributed. On the other hand, when cells were treated with PKC inhibitor alone, PLC-γ2 protein was still located in the cytoplasm. However, redistribution of PLC-γ2 protein occurred in the presence of TPA, no matter whether PKC inhibitor existed or not.CONCLUSION: PLC-γ2 translocation is critical in transmitting TPA signal to its downstream molecule PKCα. As an effector,PKCα directly promotes apoptosis of MGC80-3 cells.Therefore, protein translocation of PLCγ2 and PKCα is critical event in the process of apoptosis induction. | Bing Zhang Qiao Wu Xiao-Feng Ye Su Liu Xiao-Feng Lin Mu-Chuan Chen, Key Laboratory of the Ministry of Education for Cell Biology and Tumor Cell Engineering, School of Life Sciences, Xiamen University, Xiamen 361005, Fujian Province, China Bing Zhang, Medical school, Xiamen University, Xiamen 361005, Fujian Province. China | 2003 | World Journal of Gastroenterology2003，9，11： | 8 |
| 4 | Moleucle action mechunisms of NM-3 on human gastric cancer SGC-7901 Cells in vivo or in vitro显示文摘AIM: To study the moleucle action mechunisms of NM-3 on the growth of human gastric cancer SGC-7901 cells in vivo or in vitro.METHODS: SGC-7901 from human non-differentiated gastric cancer cell line was cultured with NM-3 at 100 mg/ml for 24 h. We observed its inhibitory rate and the density of micro-vascular growth in grafted mice with human gastric cancer SGC-7901. The apoptosis of human gastric cancer SGC-7901 was revealed in NM-3 treatment group by using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-fluorescene nick end labeling (TUNEL)method and flow cytometry analysis.RESULTS: The growth of SGC-7901 cells was markedly inhibited compared with control growp, which was smaller than that in normal saline control group (4.17 g±0.22 g VS 9.45 g±1.38 g, P<0.01). The level of apoptosis of human gastric cell line SGC-7901 was obviously increased in NM-3treatment group at 1 mg.L-1 for 24 h. NM-3 inducing apoptotic index in NM-3 plus carboplatin group was 3.5 times that of carboplatin control group (TUNEL: 27.98±6.12 % VS 12.94±2.12 %, FACScan: 26.86±5.69 % VS11.86±1.09 %,P<0.01). Western blot analysis showed that the apoptotic index of human gastric cancer was elevated for 12, 24 and 36 h with an evident time-effect relationship in groups at 100 mg.L-L. NM-3 enhanced the inhibitive effects and sensitivity of chemotherapy for human gastric cancer in nude mice. These results suggested that NM-3 played a key inhibitive role in the growth of grafted human gastric cancer in nude mice.CONCLUSION: NM-3 can inhibit the growth of human gastric cancer cell line SGC-7901, and enhance the sensitivity of carboplatin on SGC-7901 and induced its apoptosis. | Jin-Shui Zhu Bo Shen Jin-Lian Chen Guo-Qiang Chen Xiao-Hu Yu Hua-Fang Yu Zu-Ming Zhu, Affiliated Sixth People’s Hospital, Shanghai Jiaotong University, Shanghai 200233, China Guo-Qiang Chen, Shanghai Experimental Animal Center, Chinese Academy of Sciences, Shanghai 200233, China | 2003 | World Journal of Gastroenterology2003，9，10： | 8 |
| 5 | Proteomics-based Identification of Proteins with Altered Expression Induced by 12-O-Tetradecanoylphorbol 13-acetate In Nasopharyngeal Carcinoma CNE2 Cells显示文摘Nasopharyngeal carcinoma (NPC) is a malignancy with high incidence in Southern China and South-East Asia. Etiology studies indicate that chemical carcinogen promoters, such as 12-O-tetradecanoylphorbol-13-acetate (TPA), are important factors causing NPC development. However, the mechanism of the TPA effect on NPC remains unclear. In the present study, cells from a poorly differentiated squamous cell carcinoma NPC cell line, CNE2, were stimulated by TPA and proteomics technology was carried out to find protein discrepancies between control and TPA-treated cells. Results revealed that TPA treatment in CNE2 cells could upregulate the expression of ''''triosephosphate isomerase'''' and ''''14-3-3 protein sigma'''' and downregulate the expression of ''''reticulocalbin 1 precursor'''', ''''nucleophosmin'''', ''''mitochondrial matrix protein pl precursor'''', and ''''stathmin''''. The changes in the expression of these genes suggested that TPA induced CNE2 cells to antiproliferation and to apoptosis, which was confirmed by subsequent apoptosis detection. Therefore, the effects of TPA on nasopharyngeal carcinoma cells were distinct from the effects on primary epithelial cells and we suggest reasons for these differences. | Pei-ZhouJIANG MingGAN HuaHUANG Xin-MingSHEN ShuangWANG Kai-TaiYAO | 2005 | Acta Biochimica et Biophysica Sinica2005，37，2： | 5 |
| 6 | 细胞凋亡与胃癌显示文摘胃癌是我国最常见的恶性肿瘤之一 ,死亡率占恶性肿瘤的第一位。胃癌的发生与胃粘膜上皮细胞和胃癌细胞凋亡、增殖调控失衡有关。现综述细胞凋亡及凋亡相关基因在胃癌的发生、发展。 | 程磊 王跃 | 2004 | 国外医学(临床生物化学与检验学分册)2004，25，3： | 5 |
| 7 | Do there exist synergistic antitumor effects by coexpression of herpes simplex virus thymidine kinase with cytokine genes on human gastric cancer cell line SGC7901?显示文摘AIM: To evaluate the synergistic antitumor effects of herpes simplex virus thymidine kinase (HSV-TK) together with tumor necrosis factor alpha (TNF-α) or interleukin-2 (IL-2) gene expression on gastric cancer cell line SGC7901. METHODS: Recombinant vectors pL(TT)SN and pL(TI)SN,which express TK-IRES-TNF-α and TK-IRES-IL-2 genes separately, as well as the control plasmids pL(TK)SN and pLXSN were employed to transfect PA317 cells respectively to generate the viruses that can stably express the objective genes through G418 selection. The gastric cancer cells were then transfected by the retroviral serum from the package cells and maintained in culture to determine the cell growth and apoptosis. The cytotoxic effects of HSV-TK together with TNF-α or IL-2 gene expression on the transfected cancer cells were evaluated by the cell viability and bystander effects in the presence of GCV supplemented in the cultural medium. RESULTS: Expression of recombinant proteins including TNF-α and IL-2 by stable transfectants was confirmed by Western blotting. The percentage of cell apoptosis in the SGC/0, SGC/TK-TNF-α SGC/TK-IL-2 and SGC/TK done was 2.3%, 12.3%, 11.1% and 10.9% respectively at 24 h posttransfection. Cell growth status among all the experimental groups as judged by cell absorbance (A) at 570nm did not exhibit any significant difference (P>0.05); although it was noted to be slightly lower in the SGC/TT group. Cell survival rate in SGC/TI, SGC/TT and SGC/TK group was significantly decreased in a dose-dependent manner of GCV compared with that of the SGC/0 group (P<0.05-0.01). Among all studied cells, the SGC/TT was shown most sensitive to GCV with a half lethal dose of 0.5 mg.L^-1. In contrast, the survival rate of SGC/0 cells was not affected by the presence of GCV with the doses less than 10 mg-L^-1 The half lethal dose of GCV for SGC/0 cells was more than 100 mg-L^-1. Marked bystander effect induced by SGC/TI, SGC/TT and SGC/TK cells was confirmed by the fact that 20% of these stable transfectants could kill 50% of the co-cultured cells, in which the most prominent bystander effect was found in the circumstance of SGC/TT presence. However, no significant difference of these variables was found among SGC/TI,SGC/TT and SGC/TK cells (P>0.05). CONCLUSION: The synergistic antitumor effects produced by the co-expression of HSV-TK with TNF-α or IL-2 geneswere not present in the transfected SGC7901 cells. The mechanism underlying these phenomena was not known. | Jian-HuaZhang Ming-XiWan Jia-YingYuan Bo-RongPan | 2004 | World Journal of Gastroenterology2004，10，1： | 5 |
| 8 | Isolation of a novel member of small G protein superfamily and its expression in colon cancer显示文摘AIM: APMCF1 is a novel human gene whose transcripts are up-regulated in apoptotic MCF-7 cells. In order to learn more about this gene′s function in other tumors, we cloned its full length cDNA and prepared its polyclonal antibody to investigate its expression in colon cancers with immunohistochemistry.METHODS: With the method of 5′ rapid amplification of cDNA end (RACE) and EST assembled in GenBank, we extended the length of APMCF1 at 5′ end. Then the sequence encoding the APMCF1 protein was amplified by RT-PCR from the total RNA of apoptotic MCF-7 cells and cloned into the prokaryotic expression vector pGEX-KG to construct recombinant expression vector pGEX-APMCF1. The GSTAPMCF1 fusion protein was expressed in E. coli and used to immunize rabbits to get the rabbit anti-APMCF1 serum. The specificity of polyclonal anti-APMCF1 antibody was determined by Western blot. Then we investigated the expression of Apmcf1 in colon cancers and normal colonic mucosa with immunohistochemistry.RESULTS: A cDNA fragment with a length of 1 745 bp was obtained. APMCF1 was mapped to chromosome 3q22.2and spanned at least 14.8 kb of genomic DNA with seven exons and six introns contained. Bioinformatic analysis showed the protein encoded by APMCF1 contained a small GTP-binding protein (G proteins) domain and was homologous to mouse signal recognition particle receptor β(SRβ). A coding region covering 816 bp was cloned and polyclonal anti-APMCF1 antibody was prepared successfully.The immunohistochemistry study showed that APMCF1 had a strong expression in colon cancer.CONCLUSION: APMCF1 may be the gene coding human signal recognition particle receptor β and belongs to the small-G protein superfamily. Its strong expression pattern in colon cancer suggests it may play a role in colon cancer development. | Wei Yan Wen-Liang Wang Feng Zhu Sheng-Quan Chen Qing-Long Li Li Wang, Department of Patholology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi Province, China | 2003 | World Journal of Gastroenterology2003，9，8： | 4 |
| 9 | 氧化砷诱导胃癌细胞凋亡的信号传导途径研究显示文摘目的 检测氧化砷 (As2 O3 )诱导胃癌细胞株 (SGC 790 1和MKN 4 5 )凋亡过程中cAMP、蛋白激酶C(PKC)和酪氨酸蛋白激酶 (PTK)活性变化 ,以探讨其诱导胃癌细胞凋亡过程中可能存在的信号传导途径。方法 应用钙离子拮抗剂、PKC和PTK抑制剂研究其对As2 O3 诱导胃癌细胞凋亡过程的影响 ,以TUNEL法检测细胞凋亡率。以放射免疫法测定As2 O3 作用前后细胞内cAMP水平的变化。抽提PKC和PTK蛋白 ,以Lowry法测定As2 O3 作用前后各自蛋白表达水平的变化。结果 钙离子拮抗剂对As2 O3 诱导胃癌细胞凋亡过程没有影响 ,PKC和PTK抑制剂不仅本身能诱导胃癌细胞凋亡 ,且对As2 O3 诱导胃癌细胞凋亡具有协同作用。在As2 O3 诱导胃癌细胞凋亡过程中存在cAMP浓度增高和PKC、PTK活性显著降低 ,提示cAMP、PKC和PTK可能参与As2 O3 诱导胃癌细胞凋亡的作用。结论 PKC和PTK抑制剂可以通过影响信号传导系统诱导胃癌细胞凋亡 ,并能促进As2 O3 诱导胃癌细胞凋亡。 | 曹勤 涂水平 谭继宏 马天乐 乔敏敏 吴裕炘 江石湖 | 2004 | 中华消化杂志2004，24，7： | 3 |
| 10 | 雌激素诱导基因PS2/TFF1在胃癌及癌前病变中的表达显示文摘目的:明确乳腺癌雌激素诱导基因PS2/TFFl在胃癌及癌前病变中的表达及其意义。方法:采用免疫组织化学方法测定121例患者(慢性浅表性胃炎20例、胃溃疡20例、不典型增生20例、不完全肠化生20例、完全肠化生21例及胃癌20例)及20名健康志愿者胃黏膜组织中PS2/TFF1蛋白的表达。结果:PS2/TFF1在慢性浅表性胃炎、胃溃疡中表达与对照组比较明显增加(慢性胃炎组 vs正常对照组P<0.01 q=7.721胃溃疡组 vs正常对照组 P<0.01 q=5.256),在不典型增生、不完全肠化生及胃癌中表达比对照组明显减低(不典型增生组 vs正常对照组P<0.01 q=8.051;不完全肠化生组 vs正常对照组P<0.01,q=11.356;胃癌组 vs正常对照组P<0.01q=8.238),在完全肠化生组PS2/TFF1表达无明显增高(20/21,95.24%),与不完全肠化生组表达(11/20,55%)相比差异显著(P<0.01 x^2=8.994)。结论:(1)PS2/TFF1蛋白在胃黏膜保护中可能起重要作用;(2)PS2/TFF1的表达缺失可能是胃肿瘤恶性转化过程中的早期事件。 | 李俊美 罗和生 姚宏昌 | 2003 | 世界华人消化杂志2003，11，9： | 3 |
| 11 | 表没食子儿茶素没食子酸酯诱导人胃癌BGC-823细胞凋亡的机制显示文摘目的:探讨表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG)对人胃癌BGC-823细胞增殖的影响及其可能的机制。方法:不同浓度EGCG单独或联合c-Jun氨基末端激酶(c-Jun N-terminal kinase,JNK)抑制剂SP600125作用BGC-823细胞后,应用MTT法检测BGC-823细胞的增殖抑制率,显微镜下观察细胞的形态学改变,FCM检测细胞凋亡率,蛋白质印迹法检测细胞中p-JNK和p-c-jun蛋白的表达情况,免疫细胞化学法检测细胞中caspase-3的表达。结果:EGCG可抑制BGC-823细胞的增殖(P<0.05),呈时间和剂量依赖效应;EGCG可诱导BGC-823细胞凋亡,细胞凋亡率呈剂量依赖效应(P<0.05);EGCG可上调BGC-823细胞中p-JNK、p-c-jun和caspase-3的表达(P<0.05)。EGCG引起的BGC-823细胞增殖抑制和caspase-3表达水平的上调可被SP600125部分抑制。结论:EGCG可诱导人胃癌BGC-823细胞凋亡,其作用机制可能与激活JNK信号转导途径并上调caspase-3的表达有关。 | 邹少娜 林敏 伍石华 王化修 陈波 罗招阳 | 2011 | 肿瘤2011，31，6： | 3 |
| 12 | 胰腺癌组织ChAT,GAD65和PKC酶活性的表达显示文摘目的:研究ChAT,GAD65和PKC酶活性在慢性胰腺炎和胰腺癌组织中表达特征及其临床病理意义。方法:胰腺癌(n=47)和慢性胰腺炎(n=10)手术切除标本经40g/L中性甲醛固定后常规制作石蜡包埋切片,ChAT,GAD65和PKC酶活性表达染色方法均为常规ABC免疫组化法。结果:胰腺癌ChAT,GAD65和PKC表达阳性率(48.9%,55.3%和57.4%)及其评分(2.2±1.4,2.2±1.2和2.1±1.6)明显高于慢性胰腺炎阳性率(0%,10.0%和10.0%)及其评分(0.2±0.4,0.6±0.9和0.6±0.9),均有显著或高度显著性差异(P<.05或P<0.01).高分化腺癌ChAT评分值明显高于低分化腺癌(P<0.05),但阳性率之间无明显差异(P>0.05);高分化腺癌GAD65,PKC表达阳性率及其评分明显低于低分化腺癌,均有显著或高度显著性差异(P<0.05或P<0.01)。酶活性表达与胰腺癌患者性别、年龄、有无转移等临床特征均无明显关系。GAD65评分与PKC评分存在高度密切关系(r=0.50,P<0.01)结论。ChAT,CAD65和PKC酶活性表达特征可能与胰腺癌发生发展及生物学行为有密切关系,均为胰腺癌重要生物学标志物。 | 杨竹林 王群伟 邓星辉 李代强 吕芳 李永国 | 2003 | 世界华人消化杂志2003，11，10： | 3 |
| 13 | Histone deacetylase inhibitor valproic acid sensitizes B16F10 melanoma cells to cucurbitacin B treatment显示文摘Cucurbitacin B (崽) 被报导与其它一起由这个代理人的联合包括黑瘤,和更有效的政体在许多肿瘤上有反增长效果在调查下面。在这研究,崽的反黑瘤效果作为一个单个代理人并且在有 valproic 酸(VPA ) 的联合, histone deacetylase (HDAC ) 的一个禁止者,在 B16F10 被评估,一根老鼠黑瘤房间线。结果证明那崽以一种剂量依赖者方式禁止了房间线的增长。然而,它是可能的支持幸存的补偿回答,包含 autophagy 的正式就职和 anti-apoptotic Bcl-2 蛋白质的 upregulation,被崽处理导致,它可能极大地减少这个代理人的 cytotoxicity。支持这,黑瘤房间被发现对有 chloroquine 的崽的联合更敏感,一个著名 autophagy 禁止者。并且导致崽的 autophagy 与 c6 月 N 终端 kinase (JNK ) 被联系激活,至少部分,自从 JNK 的抑制,由 SP600125 的活动能减轻 autophagy。当崽与 VPA 被相结合时,二药由房间 apoptosis 的正式就职显示出 synergistic cytotoxicity。而且,崽的 multiploidization 效果也面对 VPA 被压制。与由崽的 JNK 的短暂激活相对照,崽和 VPA 的联合导致了延长 JNK 激活,尽管在在 4 h 以后的底层。我们的结果证明 HDAC 禁止者 VPA 能通过 apoptotic 小径的正式就职敏化 B16F10 房间到崽处理。 | Dongyun Ouyang Yanting Zhang Lihui Xu Jingjing Li Qingbing Zha Xianhui He | 2011 | Acta Biochimica et Biophysica Sinica2011，43，6： | 3 |
| 14 | Screening and identification of mimotope of gastric cancer associated antigen MGb1-Ag显示文摘AIM: Using a monoclonal antibody against gastric cancer antigen named MGbl to screen a phage-displayed random peptide library fused with coat protein plII in order to get some information on mimotopes.lV^37BODS: Through affinity enrichment and EUSA screening,positive clones of phages were amplified. 10 phage clones were selected after three rounds of biopanning and the ability of specific binding of the positive phage clones to MGb1-Ab were detected by ELISA assay (DNA sequencing was performed and the amino acid sequences were deduced)By blocking test, specificity of the mimic phage epitopes was identified.RESULTS: There were approximately 200 times of enrichment about the titer of bound phages after three rounds of biopanning procedures. DNA of 10 phage clones after the third biopanning was assayed and the result showed that the positive clones had a specific binding activity to MGbl-Ab and a weak ability of binding to control mAb or to mouse IgG. DNA sequencing of 10 phage clones was performed and the amino acid sequences were deduced.According to the homology of the amino acid sequences of the displayed peptides, most of the phage clones had motifs of H(x)Q or L(x)S. And these 10 phage clones could also partly inhibit the binding of MGbl-Ab to gastric cancer cell KATO-Ⅲ. The percentage of blocking was from (21.0±1.6) %to (39.0±2.7) %.CONCLUSION: Motifs of H(x)Q and L(x)S selected and identified show a high homology in the mimic epitopes of gastric cancer associated antigen. There may be one or more clones which can act as candidates of tumor vaccines. | Zhe-YiHan Kai-ChunWu Feng-TianHe Quan-LiHan Yong-ZhanNie YingHan Xiao-NanLiu 3ian-YongZheng Mei-HongXu Dai-MingFan | 2003 | World Journal of Gastroenterology2003，9，9： | 2 |
| 15 | aFGF和genistein对大肠癌细胞株CCL229 PKC及ERK活性的影响显示文摘目的:观察aFGF及TPK抑制剂genistein对大肠癌细胞株CCL229细胞内PKC及ERK活性的影响,探讨其信号传导途径.方法:以不同浓度的aFGF(0.15 mg/L,0.30 mg/L,0.60mg/L,1.20 mg/L)和genistein(6.00mg/L,12.00mg/L,24.00mg/L,48.00mg/L)诱导CCL229细胞,利用[γ-^(32)P]ATP掺入外源性底物的方法,液体闪烁测定PKC及ERK活性.结果:随着aFGF浓度的增加,PKC及ERK活性随之升高,与aFGF浓度呈显著正相关(P<0.05).当aFGF浓度为1.20mg/L时,PKC(胞质),PKC(胞膜)和ERK活性分别为对照组的2.60,2.79,1.77倍.genistein抑制细胞内PKC及ERK活性,且与 genistein 浓度呈剂量依赖效应(P<0.05).当genistein浓度为48.00mg/L时,PKC(胞质),PKC(胞膜)和ERK活性分别为对照组的0.41,0.36,0.50倍.genistein对aFGF诱导的PKC及ERK活性抑制更显著.结论:大肠癌细胞株CCL229中aFGF受体具有TPK活性,TPK激活后促进蛋白质和酶磷酸化,导致PKC和ERK活性升高,进一步证明PKC及ERK确是TPK的下游信号分子. | 尚海 张颐 单吉贤 | 2003 | 世界华人消化杂志2003，11，9： | 2 |
| 16 | 佛波酯通过抑制蛋白激酶B活性诱导血管平滑肌细胞凋亡显示文摘目的探讨佛波酯对血管平滑肌细胞凋亡的影响及可能的作用机制。方法用佛波酯处理体外培养的大鼠动脉平滑肌细胞A10,原位缺口末端标记法检测佛波酯对平滑肌细胞凋亡的影响;用免疫印迹法检测蛋白激酶B及其下游底物的总蛋白和磷酸化水平。结果佛波酯可诱导平滑肌细胞的凋亡。过度表达持续活性的蛋白激酶B明显抑制佛波酯诱导的细胞凋亡;相反,显性负性蛋白激酶B加重佛波酯的促凋亡作用。进一步研究发现,佛波酯可降低蛋白激酶B的磷酸化水平,并随着剂量的增高或时间的延长而逐步降低,同时佛波酯也能抑制蛋白激酶B下游的靶蛋白如叉头转录因子3a和糖原合成酶激酶3β磷酸化水平。最后发现蛋白激酶C抑制剂可阻断佛波酯降低蛋白激酶B磷酸化水平的作用,但丝裂原活化蛋白激酶抑制剂无此作用。结论佛波酯通过蛋白激酶C信号途径抑制蛋白激酶B激酶活性而诱导平滑肌细胞凋亡。 | 范永娜 谢平 张华 郭树彬 李汇华 | 2008 | 中国动脉硬化杂志2008，16，11： | 1 |
| 17 | A 75 kDa glycoprotein isolated from Cudrania tricuspidata Bureau induces colonic epithelial proliferation and ameliorates mouse colitis induced by dextran sulfate sodium显示文摘Cudrania tricuspidata Bureau(CTB),a species of the Moraceae plant,has been used as a bruise recovery treatment.This study aimed to determine whether the 75 kDa phytoglycoprotein extracted from CTB has a regulatory effect on the proliferation of human colon epithelial cells and the pathological process of inflammatory bowel disease(IBD).We found that CTB glycoprotein significantly induces the proliferation of human colon epithelial HT-29 cells by activating protein kinase C.CTB glycoprotein stimulated the phosphorylation of c-Jun N-terminal kinase and transcription factor nuclear factor-κB,which are responsible for the expression of cell-cycle-related proteins(CDK2,CDK4,cyclin D1 and cyclin E)during its promotion of cell proliferation.Experimental colitis was induced in mice by adding dextran sulfate sodium to their drinking water at a concentration of 4%(W/V)for seven days.We found that CTB glycoprotein ameliorates the pathological process of IBD and lowers the disease activity index score,which was composed of body weight change,diarrhea,and hematochezia in ICR mice treated with dextran sulfate sodium.Hence,we suggest that CTB glycoprotein has the ability to prevent IBD by promoting cell proliferation signaling events via the activation of PKC,JNK and NF-κB in colon epithelial cells. | Park Jeong-Bae Kim Do-Wan Lim Kye-Tack Oh Sejong Lee Sei-Jung | 2021 | Chinese Journal of Natural Medicines2021，19，1： | 1 |
| 18 | 大鼠胃黏膜损伤修复时早期应答基因c-Jun 及c-met的表达显示文摘目的:建立无水乙醇性胃黏膜损伤大鼠模型并观察早期应答基因 c-Jun 和 c-met 对胃黏膜损伤修复的影响.方法:采用无水乙醇1mL 胃饲诱发急性胃黏膜损伤大鼠模型,并于伤后0,4,8d 分别处理一组大鼠,观察损伤模型自然修复过程,免疫组织化学技术检测早期应答基因 c-Jun和 c-met 的表达.结果:在损伤模型自然修复过程中,损伤后4,8d 组大鼠胃黏膜损伤指数(LI)为32±7,18±3,均显著低于损伤模型组75±11,(P<0.05);免疫组织化学显示损伤后8d 组大鼠胃黏膜 c-Jun 的阳性表达率为87.5%,显著高于正常对照组的12.5%,c-met 的阳性表达率为62.5%,均显著高于正常对照的0及损伤模型组的0(P<0.05).结论:早期应答基因 c-Jun 和 c-met 的表达能促进急性胃黏膜损伤的修复,对黏膜损伤的自愈具有重要作用. | 姚永莉 徐波 宋于刚 张万岱 | 2003 | 世界华人消化杂志2003，11，11： | 0 |
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