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| 1 | 珠子参体外诱导人肝癌细胞凋亡效应及机制研究显示文摘目的观察珠子参体外诱导人肝癌细胞凋亡效应并初探其分子机制。方法体外细胞培养采用人肝癌细胞株SMMC-7721,分为对照(BL)组、珠子参(PJ)组、二甲基亚砜(DMSO)组及5-FU组,采用电镜观察作用后肝癌细胞超微结构改变;流式细胞仪检测肝癌细胞周期和凋亡率;RT-PCR法检测癌基因c-myc、c-fos和抑癌基因p53、p21表达的变化。结果与对照组比较,电镜下珠子参组SMMC-7721细胞染色质浓缩,分解成大小不一有膜包绕团块,内含有新月形DNA物质及细胞器,形成凋亡小体;周期分析可见G0/G1期细胞阻滞,阻止了细胞向S期的转换,并引起细胞凋亡,凋亡率达38.34%;RT-PCR半定量分析珠子参能降低癌基因c-myc表达(P<0.05),增高抑癌基因p53和p21表达(P<0.05)。结论珠子参能诱导人肝癌细胞SMMC-7721凋亡,部分作用机制可能与阻滞细胞停留在G0/G1,降低癌基因c-myc和c-fos表达,增高抑癌基因p53和p21表达有关。 | 陈涛 陈龙飞 金国琴 李丹 | 2006 | 肿瘤2006，26，2： | 29 |
| 2 | PPARγ pathway activation results in apoptosis and COX-2 inhibition in HepG2 cells显示文摘AIM: To investigate whether troglitazone (TGZ), theperoxisome proliferator-activated receptor (PPAR) gammaligand, can induce apoptosis and inhibit cell proliferation inhuman liver cancer cell line HepG2 and to explore themolecular mechanisms.
METHODS: [3-(4,5)-dimethyithiazol-2-yl]-2,5-diphenyltetrazolium bromide (NTT), [3H] Thymidine incorporation,Hochest33258 staining, DNA ladder, enzyme-linkedimmunosorbent assay (ELISA), RT-PCR, Northern and Western blotting analyses were employed to investigate the effect of TGZ on HepG2 cells and related molecular mechanisms.RESULTS: TGZ was found to inhibit the growth of HepG2cells and to induce apoptosis. During the process, the expression of COX-2 mRNA and protein and Bcl-2 protein was down-regulated, while that of Bax and Bak proteins was up-regulated, and the activity of caspase-3 was elevated.Furthermore, the level of PGE2 was decreased transiently after 12 h of treatment with 30 gM troglitazone.
CONCLUSION: TGZ inhibits cell proliferation and induces apoptosis in HepG2 cells, which may be associated with the activation of caspase-3-like proteases, down-regulation of the expression of COX-2 mRNA and protein, Bcl-2 protein,the elevation of PGE2 levels, and up-regulation of the expressions of Bax and Bak proteins. | Ming-YiLi HuaDeng Jia-MingZhao DongDai Xiao-YuTan | 2003 | World Journal of Gastroenterology2003，9，6： | 25 |
| 3 | Effect of c-myc,Ki-67,MMP-2 and VEGF expression on prognosis of hepatocellular carcinoma patients undergoing tumor resection显示文摘AIM: To explore the effect of c-myc, Ki-67, MMP-2 and VEGF expression on prognosis of hepatocellular carcinoma (HCC) patients undergoing tumor resection.METHODS: Primary HCC patients underwent tumor resection were retrospectively analysed. The maximum size of the tumor was less than 5 cm, there was only one nodule in each patient. No chemoembolization was performed before resection. They were followed up after resection, and the time of recurrence was recorded. They were divided into 2 groups: group A (15 cases): tumor recurrence within 1 year after tumor resection, and group B (15 cases):with or without tumor recurrence 2 years after tumor resection. Pathological slices were made with tumor waxsample. Immunohistochemistry staining was performed with c-myc, Ki-67, MMP-2 and VEGF monoclonal antibodies.Staining intensity was quantitatively analysed with a pathological diagram-writing analyzing system. The expressing intensity differences of stained molecules in cancer tissue and para-cancer were analysed.RESULTS: c-myc, Ki-67, MMP-2 and VEGF expressing intensities in cancer tissue in group A were higher than those in group B (Pvalues were 0.010, 0.030, 0.022 and 0.004, respectively), but they were not significantly different in para-cancer tissue in groups A and B (Pvalues were 0.334, 0.343, 0.334 and 0.334, respectively).CONCLUSION: The expression of c-myc, Ki-67, MMP-2 and VEGF in cancer tissue is related to the recurrence of HCC after tumor resection. | JunCui Bao-WeiDong PingLiang Xiao-LingYu De-JiangYu | 2004 | World Journal of Gastroenterology2004，10，10： | 21 |
| 4 | Antisense oligonucleotide targeting at the initiator of hTERT arrests growth of hepatoma cells显示文摘AIM:To evaluate the inhibitory effect of antisense phosphorothioate oligonucleotide (asON) complementary to the initiator of human telomerase catalytic subunit (hTERT) on the growth of hepatoma cells.METHODS:The as-hTERT was synthesized by using a DNA synthesizer. HepG2.2.15 cells were treated with ashTERT at the concentration of 10μmol/L. After 72h, these cells were obtained for detecting growth inhibition,telomerase activity using the methods of MTT,TRAP-PCR-ELISA, respectively. BALB/c(nu/nu) mice were injected HepG2.2.15 cells and a human-nude mice model was obtained. There were three groups for anti-tumor activity study. Once tumors were established, these animals in the first group were administered as-hTERT and saline.Apoptosis of tumor cells was detected by FCM. In the 2nd group, the animals were injected HepG2.2.15 cells together with as-hTERT. In the third group, the animals were given as-hTERT 24 hours postinjection of HepG2.2.15 cells. The anti-HBV effects were assayed with ELISA in vitro and in vivo.RESULTS: Growth inhibition was observed in cells treated with as-hTERT in vitro. A significant different in the value of A570-A630 was found between cells treated with as-hTERT and control (P<0.01) by MTT method. The telomerase activity of tumor cells treated with as-hTERT was reduced,the value of A4so nm was 0.42 compared to control (1.49) with TRAP-PCR-ELISA. The peak of apoptosis in tumor cells given as-hTERT was 21.12%, but not seen in saline-treated control. A prolonged period of carcinogenesis was observed in the second and third group animals. There was inhibitory effect on the expression of HBsAg and HBeAg in vivo and in vitro.CONCLUSION: As-hTERT has an anti-tumor activity, which may be useful for gene therapy of tumors. | Su-XiaLiu Wen-ShengSun Ying-LinCao Chun-HongMa Li-HuiHan Li-NingZhang Zhen-GuangWang Fa-LiangZhu | 2004 | World Journal of Gastroenterology2004，10，3： | 20 |
| 5 | Codon 249 mutation in exon 7 of p53 gene in plasma DNA:maybe a new early diagnostic marker of hepatocellular carcinoma in Qidong risk area,China显示文摘AIM: One of the characteristics of hepatocellular carcinoma (HCC) in Qidong area is the selective mutation resulting in a serine substitution at codon 249 of the p53 gene (1,20),and it has been identified as a 'hotspot' mutation in heptocellular carcinomas occurring in populations exposed to aflatoxin and with high prevalence of hepatitis B virus carriers (2, 3, 9, 10, 16, 24). We evaluated in this paper whether this 'hotspot' mutation could be detected in cellfree DNA circulating in plasma of patients with hepatocellular carcinoma and cirrhosis in Qidong, China, and tried to illustrate the significance of the detection of this molecular biomarker.METHODS: We collected blood samples from 25hepatocellular carcinoma patients, 20 cirrhotic patients and 30 healthy controls in Qidong area. DNA was extracted and purified from 200 μl of plasma from each sample. The 249ser p53 mutation was detected by restriction digestion analysis and direct sequencing of exon-7 PCR products.RESULTS: We found in exon 7 of p53 gene G→T transversion at the third base of codon 249 resulting 249Arg→249ser mutation in 10/25 (40%) hepatocellular carcinoma cases,4/20 (20%) cirrhotics, and 2/30 (7 %) healthy controls.The adjusted odds ratio for having the mutation was 22.1(95 % CI, 3.2~91.7) for HCC cases compared to controls.CONCLUSION: These data show that the 249ser p53mutation in plasma is strongly associated with hepatocellular carcinoma in Qidong patients. We found this mutation was also detected, although it was at a much lower frequency,in plasma DNA of Qidong cirrhotics and healthy controls;We consider that these findings, together with the usual method of HCC diagnosis, will give more information in early diagnosis of HCC, and 249ser p53 mutation should be developed to a new early diagnostic marker for HCC. | Xing-HuaHuang Lu-HongSun Dong-DongLu YanSun Li-JieMa Xi-RanZhang JianHuang LongYu | 2003 | World Journal of Gastroenterology2003，9，4： | 18 |
| 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 | Peroxisome proliferator-activated receptor gamma ligands inhibit cell growth and induce apoptosis in human liver cancer BEL-7402 cells显示文摘AIM: To investigate the characteristics of PPAR gamma ligands induced apoptosis in liver cancer cells.METHODS: The effects of ligands for each of the PPAR gamma ligands on DNA synthesis and cell viability were examined in BEL-7402 liver cancer cells. Apoptosis was characterized by Hochest33258 staining, DNA fragmentation,TUNEL and ElISA, and cell cycle kinetics by FACS. Modulation of apoptosis related caspases expression by PPAR gamma ligands was examined by Western blot.RESULTS: PPARgamma ligands, 15-deoxy-12,14-prostaglandin J2 (15d-PGJ2) and troglitazone (TGZ), suppressed DNA synthesis of BEL-7402 cells. Both 15d-PGJ2 and TGZ induced BEL-7402 cell death in a dose dependent manner, which was associated with an increase in fragmented DNA and TUNEL-positive cells. At concentrations of 10 and 30 μM,15d-PGJ2 or troglitazone increased the proportion of cells with G0/G1 phase DNA content and decreased those with S phase DNA content. There was no significant change in the proportion of cells with G2/M DNA content. The activities of Caspases-3, -6, -7 and -9 were increased by 15d-PGJ2and TGZ treatment, while the activity of Caspase 8 had not significantly changed.CONCLUSION: The present results suggest the potential usefulness of PPAR gamma ligands for chemoprevention and treatment of liver cancers. | Ming-YiLi HuaDeng .lia-MingZhao DongDai Xiao-YuTan | 2003 | World Journal of Gastroenterology2003，9，8： | 16 |
| 8 | VEGF、p53和MVD在胃癌中的表达及临床意义显示文摘目的:检测胃癌组织和血清中VEGF、组织的p53、MVD的表达,并观察其与胃癌生物学行为之间的关系,以及三者的相关性。方法:应用酶联免疫技术(ABC-ELISA方法)检测73例胃癌患者术前血清和20例健康体检者血清中的VEGF表达水平,同时应用免疫组织化学染色方法检测癌组织和癌旁组织中VEGF、P53和CD34的表达。结果:胃癌患者术前血清VEGF表达水平明显高于健康体检者(VEGF:101.8±53.3ng/Lvs16.1±22.5ng/L,P<0.05)。胃癌患者术前血清VEGF表达水平随浸润深度、TNM分期、淋巴结转移、远处转移而增高(P<0.05),而与年龄、性别及病理类型无关。胃癌组织VEGF的阳性表达率为71.2%,癌旁组织中VEGF未见阳性表达,P<0.05;胃癌组织VEGF表达水平与胃癌浸润深度、TNM分期、淋巴结转移、远处转移有关(P<0.05),而与年龄、性别及病理类型无关。胃癌患者术前血清VEGF的表达水平与组织VEGF的表达呈正相关(r=0.346,P<0.01)。胃癌组织中p53的阳性表达率明显高于癌旁组织,P<0.05。p53在胃癌组织中的表达与性别、年龄、病理类型、浸润深度无关(P>0.05),与淋巴结转移、TNM分期、远处转移有关,P<0.05。MVD值在胃癌组织中明显高于胃癌癌旁组织,并与性别、年龄、病理类型无关(P>0.05),与浸润深度、淋巴结转移、TNM分期、无远处转移有关(P<0.05)。胃癌患者术前血清与组织VEGF表达水平分别与p53的表达水平呈正相关(r=0.316,P<0.01;r=0.290,P<0.05);胃癌患者术前血清与组织VEGF表达水平分别与MVD的表达水平呈正相关(r=0.434,P<0.01;r=0.512,P<0.01);胃癌患者p53与MVD的表达水平呈正相关(r=0.431,P<0.01)。结论:胃癌患者VEGF、p53与MVD胃癌的发生、发展、转移及预后起着重要的作用,有望成为胃癌术前诊断、判断转移危险的新的肿瘤标志物。 | 周红凤 吴瑾 栾英红 王雯 付冬伟 刘丹 | 2008 | 现代肿瘤医学2008，16，5： | 15 |
| 9 | 中药复方胃肠安血清诱导肝癌SMMC-7721细胞分化显示文摘目的:观察中药复方胃肠安诱导肝癌细胞分化的作用.方法:以SMMC-7721人肝癌细胞为研究对象,维甲酸为对照,采用药物血清添加法,通过 MTT法和 Alamar Blue法观察胃肠安对肝癌细胞增生的抑制作用;放射免疫法观察对肝癌细胞分泌甲胎蛋白和白蛋白的影响;Western blot观察对肝癌细胞P53、P16以及P21蛋白表达的影响.结果:MTT法显示胃肠安与维甲酸对SMMC-7721人肝癌细胞增生均有抑制作用,胃肠安在48 h达到最大,而维甲酸对细胞增生的抑制作用在48 h后逐渐下降,较胃肠安组明显降低.Alamar Blue法结果显示,16 h后,胃肠安组细胞还原的 Alamar Blue值较对照组明显减少,并在32 h后较维甲酸组显著下降,提示与维甲酸相比,胃肠安作用起效慢但持续时间长;胃肠安组分泌的甲胎蛋白较对照组显著减少(11.4 ±1.4μg/L vs 17.2 ± 1.1μg/L,P=0.036),而白蛋白显著增多(0.40 ± 0.02mg/L vs 0.29 ± 0.01mg/L,P=0.043);胃肠安组突变型P53蛋白的表达较对照组明显减少,而P16蛋白和P21蛋白的表达较对照组增多.结论:胃肠安方剂具有抑制SMMC-7721人肝癌细胞增生、诱导细胞分化的作用,其机制可能在于减少突变型P53蛋白表达和增加P16,P21蛋白表达。 | 赵海磊 刘成 赵爱光 | 2003 | 世界华人消化杂志2003，11，9： | 13 |
| 10 | Study on the mechanism of epidermal growth factor-induced proliferation of hepatoma cells显示文摘AIM: Many growth factors, such as epidermal growth factor(EGF), are associated with the carcinogenesis. EGF plays itsrole in the proliferation of hepatoma cells through bindingwith EGF receptor (EGFR) and a series of signal transduction.But the postreceptor pathway is still not clear. In the presentexperiment, we studied the effect of tyrosine kinase, proteinkinase C, Na+/H+ exchange, calmodulin and voltage-dependent Ca2+ channel on EGF-induced hepatoma cellproliferation.METHODS: Hepatoma cell line SMMC7721 was cultured inRPMI1640 serum-free medium. In order to study the effectof thyrosine kinase, protein kinase C, Na+/H+ exchange,calmodulin and voltage-dependent Ca2+ channel on humanheptoma cell proliferation induced by epidermal growth factor(EGF), DNA synthesis rate of hepatoma cells was measuredby the method of 3H-TdR incorporation.RESULTS: EGF (10-9 M) stimulated the proliferation of heptomacells significantly (3H-TdR incorporation was 1 880+281 cpm/well, P<0.05), and this effect was significantly inhibited bytyrosine kinase inhibitor genistein (3H-TdR incorporation was808±209 cpm/well, P<0.001). Calmedulin inhibitor W-7, proteinkinase C inhibitor H-7 and Na+/H+ exchange inhibitor amilorideindividually had significant inhibiting effect on EGF-inducedproliferation of hepatoma cells (3H-TdR incorporation was978±87.3 cpm/well, 1 241+147 cpm/well, 1 380+189 cpm/well, respectivly, P<0.001, P<0.01, P<0.05), but they allhad no effect on the basal level proliferation of culturedhepatoma cells (3H-TdR incorporation was 1 284+260 cpm/well, 1 179+150 cpm/well, 1 392+152 cpm/well, respectivly,3H-TdR incorporation of the control was 1353+175 cpm/well, P>0.05). Voltage-dependent Ca2+ channel inhibitorverapamil had no inhibition on EGF-induced proliferation ofhepatoma cells (3H-TdR incorporation was 1 637+133 cpm/well, P>0.05), it also had no effect on the basal levelproliferation of cultured hepatoma cells (3H-TdR incorporationwas 1196+112 cpm/well,P>0.05).CONCLUSION: Our data suggest that tyrosine kinase, Ca2+-calmodulin-dependent pathway, protein kinase C and Na+/H+ exchange play a critical role in EGF-induced proliferationof hepatoma cells and that the effect of EGF is independentof voltage-dependent Ca2+ channel. | Bin-WenWu YuanWu Jia-LongWang Ju-ShengLin Shu-YuYuan AiLi Wu-RenCui | 2003 | World Journal of Gastroenterology2003，9，2： | 11 |
| 11 | 抑癌基因蛋白表达与前列腺癌临床病理特征和转移的关系显示文摘目的 探讨抑癌基因蛋白表达与前列腺癌临床病理特征和转移的关系。方法 应用免疫组化方法检测 4 5例前列腺癌组织中 p5 3,p16和PTEN抑癌基因蛋白表达。 结果 在前列腺癌组织中 p5 3,p16和PTEN蛋白表达阳率为 4 2 .2 % (19/4 5 )、5 7.8% (2 6 / 4 5 )和 31.1% (14 / 4 5 )。p5 3,p16和PTEN蛋白表达与前列腺癌分级、分期和转移相关 (P <0 .0 5 )。 结论 p5 3。 | 谷化平 尚培中 张正猛 周翠玲 | 2005 | 山西医科大学学报2005，36，1： | 10 |
| 12 | 胃癌组织VEGF,Flt1,bFGF,P^(53)表达与胃癌预后的关系显示文摘目的:探讨胃癌中VEGF,Fltl,bFGF,P53的表达及意义方法:应用SABC免疫组化法,研究VEGF,Fltl,bFGF, P53在胃癌中表达及与胃癌生长转移、临床病理特征、预后的关系. 结果:胃癌VEGF表达与肿瘤浸润深度有关(浆膜、浆膜外vs 肌层和黏膜层,P<0.01).P53表达与淋巴结转移相关(P53 阳性淋巴结转移组vs P53阴性淋巴结无转移组,P<0.05). VEGF与Fltl表达呈正相关(VEGF表达在Fltl阳性组vs在Fltl阴性组,P<0.01);影响胃癌预后的因素有临床病理分期、VEGF表达、肿瘤浸润深度、手术方式.Kaplan-Meier 研究显示VEGF表达与胃癌生存预后相关(P<0.05).Fltl, bFGF,P53表达与生存预后无关(P>0.05). 结论:P53表达与淋巴结转移相关.VEGF表达与肿瘤浸润深度和胃癌生存预后相关,VEGF表达可作为预测胃癌预后一项很好的指标. | 段伦喜 钟德午 胡辅珍 赵华 杨竹林 易文君 舒国顺 华颂文 | 2004 | 世界华人消化杂志2004，12，3： | 8 |
| 13 | Maxizyme-mediated specific inhibition on mutant-type p53 in vitro显示文摘AIM: To evaluate the specific inhibition of maxizyme directing against mutant-type p53 gene (mtp53) at codon 249 in exon 7 (AGG→AGT)in vitro.METHODS: Two different monomers of anti-mtp53maxizyme (maxizyme right MzR, maxizyme left MzL) and control mutant maxizyme (G5→A5) were designed by computer and cloned into vector pBSKU6 (pBSKU6MzR,pBSKU6MzL). After being sequenced, the restrictive endonuclease site in pBSKU6MzR was changed by PCR and then U6MzR was inserted into pBSKU6MzL, the recombinant vector was named pU6Mz and pU6asMz (mutant maxizyme).Mtp53 and wild-type p53 (wtp53) gene fragments were cloned into pGEN-T vector under the T7 promoter control.The 32p-labeled mtp53 transcript was the target mRNA. Cold maxizyme transcripts were incubated with 32p-labeled target RNA in vitro and radioautographed after denaturing polyacrylamide gel electrophoresis.RESULTS: In cell-free systems, pU6Mz showed a specific cleavage activity against target mRNA at 37 ℃ and 25 mM MgCL2. The cleavage efficiency of pU6Mz was 42 %, while pU6asMz had no inhibitory effect. Wtp53 was not cleaved by pU6Mz either.CONCLUSION: pU6Mz had a specific catalytic activity against mtp53 in cell-free system. These lay a good fundation for studying the effects of anti-mtp53 maxizyme in HCC cell lines. The results suggest that maxizyme may be a promising alternative approach for treating hepatocellular carcinoma containing mtp53. | Xin-JuanKong Yu-HuSong Ju-ShengLin Huan-JunHuang Nan-XiaWang Nan-ZhiLiu BinLi You-XinJin | 2003 | World Journal of Gastroenterology2003，9，7： | 6 |
| 14 | P53和Sialyl Lewis-X表达与甲状腺乳头状癌侵袭转移的关系显示文摘目的 探讨甲状腺乳头状癌(PTC)组织中P53和唾液酸化路易斯- X(SLeX)蛋白表达与肿瘤侵袭、转移的关系。方法 应用免疫组织化学催化信号放大(CSA)方法,对46例PTC、20例结节性甲状腺肿(NG)、20例慢性淋巴细胞甲状腺炎(CLT)和15例正常甲状腺组织(NT)进行了 P53 和 SLeX基因蛋白检测。结果 在 PTC中,P53 和 SLeX表达阳性率分别为65.2%(30/46)和69.6%(32/46),显著高于 NG、CLT和 NT(P<0.05);P53 和 SLeX表达阳性与PTC的侵袭、转移呈显著正相关(P<0.05)。结论 P53 和 SLeX阳性表达与 PTC侵袭、转移密切相关,检测 P53 和SLeX蛋白表达可作为判断PTC预后的参考指标。 | 谷化平 李德炳 张正猛 尚培中 | 2005 | 西安交通大学学报(医学版)2005，26，1： | 6 |
| 15 | P53基因在肝癌发生中的作用新进展显示文摘 | 王子锡 | 2010 | 右江医学2010，38，2： | 5 |
| 16 | 应用基因芯片技术筛选肝细胞癌相关基因显示文摘目的:探讨基因表达谱芯片技术在筛查肝细胞癌(HCC)相关基因群表达中的作用。方法:TRIzol法抽提2例HCC及正常肝脏组织总RNA,分离纯化两种组织的mRNA;逆转录合成掺入生物素标记的cDNA合成探针,与基因芯片(涵盖了18400个转录本,代表了14 500个明晰的基因)杂交,扫描芯片荧光信号图像,计算机分析,比较2种组织基因表达谱差异。结果:2例HCC组织与正常肝脏组织相比,有2756条基因(19.01%)共同表达差异,其中共同上调基因1772条和共同下调基因984条,对2756条共同差异表达基因作了初步功能分类,这些基因与HCC的发病机制存在相关性。结论:基因表达谱芯片技术可以筛选出HCC表达异常的相关基因群,有助于认识肝癌的发病机制。 | 张弘 黄介飞 黄晓平 黄东风 魏群 鲍柏军 华婷琰 | 2007 | 世界华人消化杂志2007，15，22： | 5 |
| 17 | 磷酸化P53与ERα在乳头状甲状腺癌中的相关性研究显示文摘目的探讨磷酸化P53[p-P53(Ser 6)]与雌激素受体(ER)α在乳头状甲状腺癌(PTC)中的表达及其相关性。方法应用免疫组织化学Elivision plus二步法检测p-P53(Ser 6)、突变P53(mut-p53)、ERα在34例生育期女性乳头状甲状腺癌组织石蜡切片中的表达,并进一步分析p-P53(Ser 6)与ERα表达的相关性。结果生育期女性的PTC组织中均有p-P53(Ser 6)的的表达,阳性率为100%,表现为细胞核或细胞核/质阳性染色,其表达与mut-P53的检测结果有明显不同。生育期女性PTC组织中p-P53(Ser6)的表达水平与ERα呈显著正相关(r=0.334,P=0.053),而mut-P53的表达水平与ERα表达无相关(r=-0.078,P=0.661)。结论 p-P53(Ser6)与ERα的表达呈显著正相关,提示P53磷酸化可能参与促进了生育期女性PTC的发生、发展。 | 张亘 黄燕红 李静 | 2015 | 中国医科大学学报2015，44，1： | 5 |
| 18 | CK19,P53,P63,EMA,P170蛋白在甲状腺乳头状癌中的表达及病理意义显示文摘[目的]评价CK19,P53,P63,EMA在鉴别甲状腺良恶性(乳头状癌)病变中的临床应用价值;了解甲状腺乳头状癌P170蛋白表达的意义。[方法]通过免疫组织化学方法,检测CK19,P53,P63,EMA,及P170蛋白在38例甲状腺乳头状癌和38例甲状腺良性病变中的表达。[结果]CK19、P53、P63、EMA在甲状腺乳头状癌和良性病变中的阳性率分别为92.1%(35/38)和2.6%(1/38)(P<0.005),89.5%(34/38)和18.4%(7/38)(P<0.005),23.7%(9/38)和10.5%(4/38)(P>0.1),34.2%(13/38)和50%(19/38)(P>0.1)。甲状腺乳头状癌中P170表达阳性率为57.9%(22/38)。[结论](1)CK19和P53是甲状腺乳头状癌病理诊断中非常有价值的辅助诊断指标。(2)甲状腺乳头状癌中P170表达的阳性率与CK19的阳性程度密切相关。 | 田丰秋 吕丽 冯晓海 王乃玉 张文波 王莉芬 | 2007 | 大连医科大学学报2007，29，2： | 4 |
| 19 | HSP70和P53蛋白在甲状腺乳头状癌中的表达及其与临床病理特征的关系显示文摘目的:探讨热休克蛋白70(HSP70)和P53蛋白在甲状腺乳头状癌组织中的表达及其与临床病理特征的关系。方法:应用免疫组织化学Envision法检测35例甲状腺乳头状癌组织、15例甲状腺良性病变组织及15例正常甲状腺组织中HSP70和P53蛋白的表达,分析HSP70和P53蛋白的表达与甲状腺乳头状癌临床病理学特征的关系。结果:甲状腺乳头状癌组织中HSP7O和P53阳性表达率明显高于甲状腺良性病变组织及正常甲状腺组织(P<0.01)。HSP7O在甲状腺乳头状癌组织中的表达与是否有颈部淋巴结转移、浸润深度以及AJCC分期密切相关(P<0.01),而与年龄、性别、肿瘤的大小以及分化程度无关(P>0.05)。P53在PTC组织中的表达与组织分化程度、是否有淋巴结转移、浸润深度以及AJCC分期密切相关(P<0.01),而与年龄、性别、肿瘤的大小无关(P>0.05)。HSP70和P53蛋白在PTC组织中的表达呈正相关性(r=0.679,P<0.01)。结论:HSP70和p53蛋白在PTC中均呈高表达,并有协同作用,两者可作为预测PTC的生物学行为和预后的参考指标。 | 李延辉 夏明汗 康举龄 谢敏如 马少康 | 2011 | 现代生物医学进展2011，11，13： | 4 |
| 20 | Phosphoinositide-3-kinase,catalytic,alpha polypeptide RNA interference inhibits growth of colon cancer cell SW948显示文摘AIM:To investigate the gene knock-down effect by the phosphoinositide-3-kinase,catalytic,alpha polypeptide(PIK3CA)-targeted double-stranded RNA(dsRNA) and its effect on cell proliferation and cycle distribution in SW948.METHODS:Two PIK3CA-targeted dsRNAs were constructed and transfected into SW948 cells.Transfections were performed using lipofectamine TM 2000.The transfection effectiveness was calculated basing on the rate of fluorescence cell of SW948 at 6 h after transfection.Total messenger RNA was extracted from these cells using the RNeasy kit,and semiquantitative reverse transcription polymerase chain reaction was performed to detect the down-regulation of PIK3CA,AKT1,MYC,and CCND1 gene expression.Cells were harvested,proteins were resolved,and western blot was employed to detect the expression levels of PIK3CA,AKT1,MYC,and CCND1 gene.Cell proliferation was assessed by 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide assay and the inhibition rate was calculated.Soft agar colony formation assay was performed basing on colonies greater than 60 μm in diameter at ×100 magnification.The effect on cell cycle distribution and apoptosis was assessed by flow cytometry.All experiments were performed in triplicate.RESULTS:Green fluorescence was observed in SW948 cell transfected with plasmid Pgenesil-1,and the transfection effectiveness was about 65%.Forty-eight hours post-transfection,mRNA expression of PIK3CA in SW948 cells was 0.51 ± 0.04 vs 0.49 ± 0.03 vs 0.92 ± 0.01 vs 0.93 ± 0.03(P = 0.001) in Pgenesil-CA1,Pgenesil-CA2,negative and blank group respectively.mRNA expression of AKT1 was 0.50 ± 0.03 vs 0.48 ± 0.01 vs 0.93 ± 0.04 vs 0.92 ± 0.02(P = 0.000) in Pgenesil-CA1,Pgenesil-CA2,negative and blank group respectively.mRNA expression of MYC was 0.49 ± 0.01 vs 0.50 ± 0.04 vs 0.90 ± 0.02 vs 0.91 ± 0.03(P = 0.001) in the four groups respectively.mRNA expression of CCND1 was 0.45 ± 0.02 vs 0.51 ± 0.01 vs 0.96 ± 0.03 vs 0.98 ± 0.01(P = 0.001) in the four groups respectively.The protein level of PIK3CA was 0.53 ± 0.01 vs 0.54 ± 0.02 vs 0.92 ± 0.03 vs 0.91 ± 0.02(P = 0.001) in Pgenesil-CA1,Pgenesil-CA2,negative and blank group respectively.The protein level of AKT1 in the four groups was 0.49 ± 0.02 vs 0.55 ± 0.03 vs 0.94 ± 0.03 vs 0.95 ± 0.04,P = 0.000).The protein level of MYC in the four groups was 0.51 ± 0.03 vs 0.52 ± 0.04 vs 0.92 ± 0.02 vs 0.95 ± 0.01(P = 0.000).The protein level of CCND1 in the four groups was 0.54 ± 0.04 vs 0.56 ± 0.03 vs 0.93 ± 0.01 vs 0.93 ± 0.03(P = 0.000).Both Pgenesil-CA1 and Pgenesil-CA2 plasmids significantly suppressed the growth of SW948 cells when compared with the negative or blank group at 48 h after transfec-tion(29% vs 25% vs 17% vs 14%,P = 0.001),60 h after transfection(38% vs 34% vs 19% vs 16%,P = 0.001),and 72 h after transfection(53% vs 48% vs 20% vs 17%,P = 0.000).Numbers of colonies in negative,blank,CA1,and CA2 groups were 42 ± 4,45 ± 5,8 ± 2,and 10 ± 3,respectively(P = 0.000).There were more than 4.5 times colonies in the blank and negative control groups as there were in the CA1 and CA2 groups.In addition,the colonies in blank and negative control groups were also larger than those in the CA1 and CA2 groups.The percentage of cells in the CA1 and CA2 groups was significantly higher in G 0 /G 1 phase,but lower in S and G 2 /M phase when compared with the negative and control groups.Moreover,cell apoptosis rates in the CA1 and CA2 groups were 5.11 ± 0.32 and 4.73 ± 0.32,which were significantly higher than those in negative(0.95 ± 0.11,P = 0.000) and blank groups(0.86 ± 0.13,P = 0.001).No significant difference was found between CA1 and CA2 groups in cell cycle distribution and apoptosis.CONCLUSION:PIK3CA-targeted short hairpin RNAs can block the phosphoinositide 3-kinase-Akt signaling pathway and inhibit cell growth,increase apoptosis,and induce cell cycle arrest in the PIK3CA-mutant colon cancer SW948 cells. | Wen-Sheng Huang Tian-Bao Wang Yao He Yu-Jun Chen Shi-Long Zhong Min Tan | 2012 | World Journal of Gastroenterology2012，18，26： | 4 |
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