|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Risk factors for early recurrence of small hepatocellular carcinoma after curative resection显示文摘BACKGROUND:Poorer prognosis is seen in patients with hepatocellular carcinoma (HCC) after curative hepatic resection with early recurrence (≤1 year) than in those with late recurrence (>1 year).This study aimed to identify risk factors for postoperative early recurrence of small HCC (≤3 cm in diameter).METHODS:The study population consisted of 158 patients who underwent curative resection for small HCC between January 2002 and July 2004.Risk factors for early recurrence were analyzed.RESULTS:Thirty-three (20.8%) patients developed early recurrence after surgery.Univariate analysis showed the following significant risk factors for early recurrence in small HCC:serum alpha-fetoprotein (AFP) level >100 ng/ml,lack of tumor capsule formation,microscopic vascular invasion,high Edmonson-Steiner grades,and cytokeratin-19 (CK-19) expression (P<0.05).Multivariate stepwise logistic regression analysis showed that serum AFP level >100 ng/ml (odds ratio 2.561,95% confidence interval 1.057 to 6.206,P=0.037) and microscopic vascular invasion (odds ratio 4.549,95% confidence interval 1.865 to 11.097,P=0.001) were independent factors.CONCLUSIONS:Postoperative early recurrence is related to serum AFP level >100 ng/ml and microscopic vascular invasion in patients with small HCC.Adjuvant therapy and careful follow-up are required for patients with these risk factors. | Zhou, Yan-Ming Yang, Jia-Mei Li, Bin Yin, Zheng-Feng Xu, Feng Wang, Bin Xu, Wen Kan, Tong | 2010 | Hepatobiliary & Pancreatic Diseases International2010，9，1： | 24 |
| 2 | Elevated serum alpha fetoprotein levels promote pathological progression of hepatocellular carcinoma显示文摘AIM:To investigate the biological role of alpha fetoprotein (AFP) and its clinical signif icance in carcinogenesis of hepatocellular carcinoma (HCC).METHODS:Clinical analysis of HCC patients and im-munohistochemical examination were conducted to evaluate the relationship between serum AFP level and patient mortality. Confocal microscopy,Western blotting, dimethylthiahzolyl-2,5-diphenyl-tetrazolium bromide,Cell Counting Kit-8 assays and flow cytometry were performed to explore the possible mechanism.RESULTS: Among the 160 HCC patients enrolled in this study,130 patients survived 2 years (81.25%),with a survival rate of 86.8% in AFP < 2 0 μg/L group,88.9% in AFP 20-250 μg/L group,and 69.6% in AFP > 250 μg/L group, demonstrating a higher mortality rate in HCC patients with higher AFP levels. Surgical treatment was benef icial only in patients with low AFP levels.The mortality rate of HCC patients with high AFP levels who were treated surgically was apparently higher than those treated with conservative management.The results of immunohistochemistry showed that AFP and AFP receptor were merely expressed in tissues of HCC patients with positive serum AFP.Consistently,in vitro analysis showed that AFP and AFPS were expressed in HepG2 but not in HLE cells. AFP showed a capability to promote cell growth,and this was more apparent in HepG2 cells,in which the proliferation was increased by 3.5 folds. Cell cycle analysis showed that the percent-age of HepG2 cells in S phase after exposure to AFP was modestly increased.CONCLUSION:HCC patients with higher AFP levels show a higher mortality rate,which appears to be attributable to the growth promoting properties of AFP. | Peng Li Shan-Shan Wang Hui Liu Ning Li Michael A McNutt Gang Li Hui-Guo Ding | 2011 | World Journal of Gastroenterology2011，17，41： | 23 |
| 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 | 甲胎蛋白水平与肝细胞癌预后的相关性分析显示文摘目的 探讨肝细胞癌(HCC)患者术前血清甲胎蛋白表达水平与外科治疗后的预后关系.方法 回顾性分析779例外科治疗HCC患者的临床资料,采用Kaplan-Meier法进行生存分析,应用Cox比例风险模型进行多因素回归分析.结果 应用ROC曲线获得中国医学科学院肿瘤医院HCC患者血清甲胎蛋白(AFP)的临界值为18.98 μg/L,此时AFP灵敏度为54.6%,特异度为82.0%.AFP阴性组(AFP <20 μg/L)术后1、3、5年生存率分别为94.4%,77.3%和58.9%;AFP阳性组(AFP≥20 μg/L)术后1、3、5年生存率分别为90.6%,64.5%和49.6% (P =0.005).Kaplan-Meier单因素分析显示:无临床症状、无腹水、小肝癌(直径≤5 cm)、肿瘤单发、血清AFP低水平表达、血清碱性磷酸酶(ALP)低水平表达、病理分化程度好、病理无脉管瘤栓、无/轻度肝硬化、Child-Pugh A级、无围手术期输血、无腹腔淋巴结转移、无大血管侵犯以及无肿瘤破裂或肝外侵犯是肝癌患者术后较好的预后因素.Cox多因素分析显示:有无临床症状、年龄、肿瘤数目、血清AFP表达水平、血清ALP表达水平、Child-Pugh分级、病理脉管瘤栓、有无腹腔淋巴结转移、有无大血管侵犯、有无肿瘤破裂或肝外侵犯以及术中输血是影响HCC患者长期生存的独立影响因素.分别以阈值1、2、3、5年为界,将总病例分为生存时间大于阈值组及小于阈值组,秩和检验结果表明:血清AFP低表达(18.3 ~23.9μg/L)具有较好的预后,血清AFP> 59.3 μg/L患者预后较差,AFP的高表达与患者的不良预后相关,并且血清AFP越高表达患者预后越差(P=0.001).结论 AFP高表达预示着肿瘤生物学行为较差、肿瘤负荷较大、肝脏背景较差、手术难度和风险及输血比例增加.血清AFP阴性表达患者具有较好的预后,血清AFP表达浓度越高预示患者预后越差. | 毕新宇 阎涛 赵宏 赵建军 李智宇 黄振 周健国 蔡建强 | 2014 | 中华医学杂志2014，94，34： | 18 |
| 5 | Therapeutic polypeptides based on HBcAg_(18-27) CTL epitope can induce antigen-specific CD_8^+ CTL-mediated cytotoxicity in HLA-A2 transgenic mice显示文摘To explore how to bigger an HLAI-restricted CD8+ T cellresponse to exogenously synthesized polypeptides in vivo. | Tong-DongShi Yu-ZhangWu Zheng-CaiJia WeiZhou Li-YunZou | 2004 | World Journal of Gastroenterology2004，10，8： | 17 |
| 6 | 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 |
| 7 | 甲胎蛋白与肝癌免疫的研究进展显示文摘肝癌是常见的消化道恶性肿瘤,目前没有较好的治疗措施。甲胎蛋白在肝癌细胞中高表达,除了用于肝癌诊断外,其作为肿瘤相关抗原已成为肝癌免疫治疗的靶点。虽然甲胎蛋白免疫原性较弱,并通过抑制树突状细胞,自然杀伤细胞以及T淋巴细胞功能促进肝癌细胞免疫逃逸,但其在肝癌免疫治疗中的作用也日益受到重视,通过体外修饰增强其免疫原性促进免疫应答,从而提高杀伤肝癌细胞免疫效应。甲胎蛋白在肝癌发生、发展及免疫中的作用为研究其在肝癌中的免疫治疗奠定了良好的基础。 | 赵倩 王小平 胥冰 蔺焕萍 张克佩 | 2016 | 生物学杂志2016，33，2： | 12 |
| 8 | 甲胎蛋白在肝癌细胞免疫逃避中的作用机制显示文摘甲胎蛋白(AFP)复杂的结构决定其在肝癌细胞生长过程中扮演多功能的角色。AFP不仅具有促进肝癌细胞增生的作用,而且还具有抑制肿瘤患者的免疫应答作用。最近研究表明AFP能损伤肝癌患者树突状细胞(DCs)的功能和诱导DCs凋亡;AFP可能通过调节DCs表型分子的表达,抑制DCs转变为成熟的抗原提呈细胞(APC)以及通过影响淋巴细胞或肝癌细胞的肿瘤坏死因子(TNF)家族及其受体的表达,抑制癌细胞内Caspase活性,导致肝癌细胞逃避机体免疫监视。 | 李孟森 李刚 | 2006 | 肿瘤研究与临床2006，18，7： | 9 |
| 9 | 原发性肝癌与甲胎蛋白研究进展显示文摘 | 辛永宁 宣世英 | 2007 | 临床肝胆病杂志2007，23，2： | 9 |
| 10 | 甲胎蛋白抑制PTEN活性导致肝癌细胞耐受ATRA诱导的凋亡显示文摘研究甲胎蛋白(α-fetoprotein,AFP)对肝癌细胞内PTEN/AKT信息通路信号传递的影响.用Western blotting法分析全反式维甲酸(all trans retinoic acid,ATRA)处理人肝癌Bel 7402和HepG2细胞24 h后PTEN表达的变化.免疫共沉淀(Co-IP)技术研究AFP与PTEN相互作用.激光共聚焦显微镜观察AFP与PTEN在细胞共定位.RNA干扰(RNAi)技术抑制AFP表达,再用ATRA处理24 h后检测细胞内PTEN表达的变化,并分析蛋白激酶B(AKT)的磷酸化.用pcDNA3.1质粒和人afp基因连接构建表达AFP的载体(称为pcDNA3.1-afp),然后转染到不表达AFP的人肝癌HLE细胞.结果显示,人肝癌Bel 7402和HepG2细胞均有PTEN的表达,ATRA(160μmol/L)处理24 h后能促进这些细胞的PTEN表达.Co-IP技术研究发现AFP能与PTEN结合.共聚焦显微镜观察显示AFP与PTEN共定位于细胞浆.干扰AFP表达后,PTEN表达明显提高.抑制AFP表达后,ATRA能显著促进Bel 7402细胞内PTEN的表达,并能抑制AKT的磷酸化.转染pcDNA3.1-afp载体后,HLE细胞内有AFP表达,并与PTEN结合,且发现pcDNA3.1-afp载体能增加AKT的磷酸化[p-AKT(Ser473)],对抗ATRA抑制HLE细胞增殖.研究的结论是:肝癌细胞内表达的AFP能与PTEN结合并抑制PTEN对AKT的去磷酸化作用,肝癌细胞内高表达的AFP能激活AKT信息通路.胞浆内的AFP是肝癌细胞耐受ATRA的重要因子. | 朱明月 符史干 李孟森 谢协驹 李刚 | 2011 | 生物化学与生物物理进展2011，38，3： | 9 |
| 11 | 鱼脑石药学研究概况显示文摘在广泛文献检索基础上,对鱼脑石的来源、鉴别、成分、临床应用等进行了综述,为其今后进一步发展提供资料依据。 | 赵婷 高昂 巩江 程亮 李娜 王明 张新刚 曹梦晔 倪士峰 | 2011 | 辽宁中医药大学学报2011，13，9： | 8 |
| 12 | 影响肝癌术后复发危险因素的研究进展显示文摘原发性肝癌(primary hepatic carcinoma,PHC)是世界上最常见且恶性程度最高的肿瘤之一,发病率在恶性肿瘤中位居世界第五位,死亡率位居第三位[1]。每年造成大约100万人死亡,其中以东亚与非洲的发病率最高,中国的PHC患者占全球患者总数的40%~50%[2]。尽管肝移植手术已经趋于成熟,而且对于伴有肝硬化的肝癌患者而言,是一种更好的选择,能带来治愈的希望,但由于供肝的紧缺,肝切除仍然是目前治疗肝癌的首选手术方式[3]。随着外科技术的逐渐提高和围手术期的各项治疗的完善, | 孙鋆泽 陆华虎 吕凌 张峰 | 2011 | 中华临床医师杂志(电子版)2011，5，11： | 7 |
| 13 | A new cytokine:the possible effect pathway of methionine enkephalin显示文摘AIM: To investigate experimentally the effects of methionineenkephalin on signal transduction of mouse myeloma NS-1cells.METHODS: The antigen determinate of delta opioidreceptor was designed in this lab and the polypeptidefragment of antigen determinate with 12 amino acidsresidues was synthesized. Monoclonal antibody against thispeptide fragment was prepared. Proliferation of Mouse NS-L cells treated with methionine enkephalin of 1x10-6 mol.L-1was observed. The activities of protein kinase A (PKA) andprotein kinase C (PKC) were measured and thereby themechanism of effect of methionine enkephalin was postulated.RESULTS: The results demonstrated that methionineenkephalin could enhance the proliferation of NS-1 cells andthe effect of methionine enkephalin could be particularlyblocked by monoclonal antibody. The activity of PKA wasincreased in both cytosol and cell membrane. With referenceto PKC, the intracellular activity of PKC in NS-1 cells waselevated at 1x10-7 mol.L-1 and then declined gradually asthe concentration of methionine enkephalin was raised. Theeffects of methionine enkephalin might be reversed by bothnaloxone and monoclonal antibody.CONCLUSION: Coupled with the findings, it in-dicates thatthe signal transduction systems via PKA and PKC are involvedin the effects of methionine enkephalin by binding with thetraditional opioid receptors, and therefore resulting in differentbiological effects. | Xin-HuaLiu Dong-AiHuang Fei-YiYang Yan-ShengHao Guo-GuangDu Ping-FengLi GangLi | 2003 | World Journal of Gastroenterology2003，9，1： | 7 |
| 14 | 大鼠不同发育时期胰腺相关蛋白的差异表达显示文摘探讨大鼠胰腺不同发育时期相关蛋白的差异表达 ,应用显微技术分离了大鼠孕 15 5天 ,孕 18 5天胚胎胰腺和新生鼠及成年鼠的胰腺 ,提取其蛋白质后 ,用固相pH梯度双向聚丙烯酰胺凝胶电泳和质谱分析等蛋白质组学方法 ,得到了 4个不同发育时期的蛋白质表达谱 .对其中的 6个在孕 18 5天胚胎胰腺中有高丰度表达 ,而在成年鼠胰腺中缺失的蛋白质点 ,4个在成年胰腺中特异表达的蛋白质点 ,8个在成年胰腺中表达明显下调的蛋白质点和 1个在成年中表达上调的点 ,进行了肽质量指纹分析和蛋白质鉴定 ,共获得 18个点的肽质量指纹图 .经BIOWORK等软件搜索大鼠非冗余蛋白质数据库来鉴定其身份 ,发现其中 7个点为大鼠甲胎蛋白 (AFP)、 5个点为胰脂酶相关蛋白 1前体、 1个点为微管蛋白 β、 2个点为蛋白二硫异构酶、 1个为FLN2 9基因产物的类似物、 1个为胰蛋白酶V A前体、 1个为过氧化物氧化还原酶 4 .其中AFP为特异表达于大鼠胚胎期及新生期胰腺的蛋白质 ,在孕 18 5天的胰腺中表达量最高 ,在成年胰腺中极低表达 . | 周锦勇 胡静静 仲燕 刘超 柴伟栋 袁栎 滕丽萍 德伟 | 2004 | 生物化学与生物物理进展2004，31，12： | 6 |
| 15 | AFP检测的临床意义及生物学作用研究新进展显示文摘 | 张国英 梁建芳 赵中夫 | 2005 | 长治医学院学报2005，19，2： | 5 |
| 16 | 甲胎蛋白对耐药基因MDR1表达及肝癌细胞化疗敏感性的影响显示文摘目的探讨甲胎蛋白(AFP)对耐药基因MDR1表达和肝癌细胞化疗敏感性的影响。方法建立稳定表达AFP的肝癌细胞系SMMC-7721/AFP,分别通过Real-timePCR和蛋白印迹检测转染前后AFP和MDR1的表达。MTF法测定SMMC-7721/AFP和SMMC-7721/EGFP细胞对阿霉素的化疗敏感性。siRNA沉默SMMC-7721/AFP细胞中MDR1的表达,观察细胞对阿霉素化疗敏感性的变化。采用免疫组织化学染色法检测60例肝癌组织中MDR1编码蛋白PgP的表达,分析PgP表达与血清AFP水平的相关性。结果在SMMC-7721/AFP细胞能检测到AFPmRNA和蛋白表达,而对照细胞则未检测到AFP表达,表明AFP稳转细胞系构建成功。SMMC-7721/AFP细胞中MDR1mRNA和蛋白水平明显高于对照细胞,SMMC-7721/EGFP和SMMC-7721/AFP细胞MDR1mRNA水平为对照组的(52.7±1.5)倍(P〈0.05)。SMMC-7721/AFP细胞对阿霉素的耐药性增加了(12.8±1.1)倍(P〈0.05)。siRNA沉默SMMC-7721/AFP细胞中MDR1的表达后细胞对阿霉素的化疗敏感性明显增强。肝癌组织中Pgp的表达和血清AFP水平呈正相关。结论AFP可通过上调MDR1的表达引起肝癌细胞对阿霉素耐药。 | 吴超 杨健 张金玲 金涛 何前进 李常海 | 2015 | 中华肝胆外科杂志2015，21，12： | 5 |
| 17 | 甲胎蛋白维持肝癌细胞恶性增生的作用机制显示文摘最近研究发现甲胎蛋白 (AFP)对肝癌等肿瘤细胞的生长有促进作用。其作用机制是 :可通过细胞膜上的AFP受体介导 ,影响淋巴细胞或肝癌细胞的肿瘤坏死因子 (TNF)家族及其受体的表达 ,导致肝癌细胞逃避机体免疫监视 ,同时又能促进癌基因表达 ,引起肝癌细胞生长。 | 李孟森 周升海 | 2003 | 国外医学(肿瘤学分册)2003，30，6： | 5 |
| 18 | Preparation and characteristics of DNA-nanoparticles targeting to hepatocarcinoma cells显示文摘AIM:To prepare thymidine kinase gene (TK gene) nanopartides and to investigate the expression of TK gene.METHODS: Poly(D,L-lactic-co-glycolic acid) (PLGA), a biodegradable and biocompatible polymer, was used to prepare recombinant plasmid p^EGFP-AFP nanoparticles by a double-emulsion evaporation technique. Characteristics of the nanoparticles were investigated in this study, including morphology, entrapment efficiency, and tissue distribution.The expression of TK gene was also investigated by MTT assay, by which the viable cells were determined alter the addition of ganciclovir (GCV).The enhanced green fluorescent protein (EGFP) expression in human hepatocellular carcinoma SMMC-7721 cells and normal parenchymal Chang liver cellswere assessed by flow cytometry.RESULTS: The prepared plasmid-nanoparticles had regular spherical surface and narrow particle size span with a mean diameter of 72±12nm.The mean entrapment efficiency was 91.25%. A total of 80.14% DNA was found to be localized in the livers after 1-h injection with ^32P-DNA-PLGA nanoparticles in mouse caudal vein. The expression of DNA encapsulated in nanopartides was much higher than that in naked DNA, and human hepatocellular carcinoma SMMC-7721 cells were more sensitive to GCV than human normal parenchymal Chang liver cells.CONCLUSION:The enhanced transfection efficiency and stronger ability to protect plasmid DNA from being degraded by nucleases are due to nanoparticles encapsulation. | QinHe JiLiu XunSun Zhi-RongZhang | 2004 | World Journal of Gastroenterology2004，10，5： | 4 |
| 19 | Effect of staurosporine on cycle of human gastric cancer cells显示文摘AIM:To study the effect of staurosporine (ST) on the cell cycle of human gastric cancer cell lines MGC803 and SGC7901.METHODS:Cell proliferation was evaluated by trypan blue dye exclusion method.Apoptotic morphology was observed under a transmission electron microscope.Changes of cell cycle and apoptotic peaks of cells were determined by flow cytometry. Expression of p21^WAF1 gene was examined using immunohistochemistry and RT-PCR.RESULTS:The growth of MGC803 and SGC7901 cells was inhibited by ST.The inhibitory concentrations against 50% cells (IC50) at 24 h and 48 h were 54ng/ml and 23ng/ml for MGC803, and 61ng/ml and 37ng/ml for SGC7901.Typical apoptotic bodies and apoptotic peaks were observed 24h after cells were treated wth ST at a concentration of 200ng/ml.The percentage of cells at G0/G1 phase was decreased and that of cells at G2/M was increased significantly in the group treated wth ST at the concentrations of 40ng/ml,60ng/ml,100ng/ml for 24h,compared with the control group (P<0.01).The expression levels of p21^WAF1 gene in both MGC803 and SGC7901 cells were markedly up-regulated after treatment with ST.CONCLUSION:ST can cause arrest of gastric cancer cells at G2/M phase,which may be one of the mechanisms that inhibit cell proliferation and cause apoptosis in these cells.Effect of ST on cells at G2/M phase may be attributed to the up-regulattion of p21^WAF1 gene. | Min-WenHa Ke-ZuoHou Yun-PengLiu YuanYuan | 2004 | World Journal of Gastroenterology2004，10，2： | 4 |
| 20 | 甲胎蛋白:治疗肝癌的新靶点显示文摘甲胎蛋白(Alpha fetoprotein,AFP)在肝癌发生过程中所起的生物学作用一直是个谜。由于其是肝癌细胞高特异性表达的蛋白质,临床上作为诊断肝癌的金标准,但是AFP在肝癌发生过程有何功能并不清楚。最近我们的研究发现,AFP具有信息调控分子样作用,AFP不仅能与维甲酸受体-β(RAR-β)结合,阻遏RAR-β进入细胞核内调节靶基因的表达,同时也能抑制Caspase-3的活性,阻断凋亡信号的传递,更重要的是AFP激活PI3/AKT等生长信号途径,提示AFP具有抗凋亡诱导的功能,靶向抑制AFP表达能增加肝癌细胞对肿瘤坏死因子相关凋亡诱导配体(TRAIL)和全反式维甲酸(ATRA)的敏感性,新发现AFP的这些功能,预示它是肝癌细胞耐药的新靶点,为肝癌的生物治疗提供新的思路和策略。 | 朱明月 李孟森 | 2014 | 海南医学2014，25，1： | 4 |
您所在的机构暂未开通此部分的功能，请联系管理员