视黄酸对胃癌细胞恶性表型的影响

研究ｔ－ＲＡ对胃癌细胞的作用和探讨其作用机理．结果表明：１）ｔ－ＲＡ能够有效地抑制胃癌细胞的生长．２）ｔ－ＲＡ能够降低胃癌细胞在软琼脂中形成集落的能力．３）ｔ－ＲＡ能够降低胃癌细胞的粘附能力．４）ｔ－ＲＡ能够抑制胃癌细胞在裸鼠中形成肿瘤的能力．４）扫描电镜观察显示,经ｔ－ＲＡ处理后,胃癌细胞表面的微绒毛消失．以上结果表明,ｔ－ＲＡ对胃癌细胞的恶性表型有显著的抑制作用．ｔ－ＲＡ可能作为治疗胃癌的有效药物．     

莪术油对胃癌细胞SGC-7901增殖和凋亡的影响

研究莪术油影响人胃癌细胞SGC-7901增殖及凋亡的机制。采用台盼蓝拒染法检测不同剂量莪术油对胃癌细胞SGC-7901的生长抑制率;光学显微镜观察细胞的形态学变化;琼脂糖凝胶电泳检测细胞DNA片段化情况;流式细胞术检测细胞线粒体膜电位的改变、细胞凋亡率以及细胞周期分布。实验结果表明：作用48h时,最佳浓度为110μg／mL,IC50值为104．958μg／mL。DNA电泳可见有梯状条带出现,流式细胞术法显示有凋亡峰出现。莪术油可诱导胃癌SGC-7901细胞凋亡。     

LncRNA MEG8影响结肠癌细胞恶性进展

目的 探究lncRNA MEG8对结肠癌细胞增殖、侵袭和凋亡的作用,阐明其作用机制.方法 利用实时荧光定量PCR(Real Time-Quantitative PCR,RT-qPCR)检测MEG8和miR-1827表达;Western blotting和CCK-8检测蛋白表达和细胞增殖;Transwell和流式细胞术检测细胞侵袭和凋亡;双荧光素酶报告基因试验和RNA免疫沉淀反应(RNA Immunoprecipitation,RIP)验证MEG8与miR-1827结合.结果 MEG8通过结合miR-1827负调控miR-1827表达.与人正常结肠上皮细胞相比,MEG8在结肠癌细胞中表达下调,而miR-1827表达上调.过表达MEG8或干扰miR-1827抑制HT29细胞增殖和侵袭,促进凋亡.沉默miR-1827逆转干扰MEG8诱导的细胞增殖和侵袭上升,凋亡和细胞外调节蛋白激酶(extracellular regulated protein kinases,ERK)/c-Jun氨基末端激酶(c-Jun N-terminal kinase,JNK)通路活性下降.结论 Ln-cRNA MEG8通过下调miR-1827,促进ERK/JNK通路活性,阻碍结肠癌细胞HT29增殖和侵袭,促进凋亡.     

X线激发纳米TiO2对胃癌细胞SGC-7901的杀伤作用

观察X线激发纳米二氧化钛(TiO2)后对体外培养的胃癌细胞SGC—7901在不同TiO2浓度下对细胞增殖的影响。探讨其可能的抑瘤机制。首先通过MTT法测定不同浓度TiO2对细胞增殖的影响。然后通过Western blot检测凋亡相关蛋白的表达变化。MTT结果显示,通过X线激发纳米TiO2后可对胃癌SGC—7901细胞的增殖产生明显的抑制作用,呈浓度相关性,当纳米TiO2浓度为0.25 mg/mL时抑制效果最明显(抑制率)。Western结果显示实验组与对照组相比凋亡相关蛋白Bax的表达显著上调。说明X线激发的纳米TiO2可抑制胃癌SGC—7901细胞的增殖,促进凋亡发生。     

miR-96对牦牛颗粒细胞凋亡和增殖的影响

为研究牦牛卵巢组织内miR-96对颗粒细胞凋亡、增殖及激素分泌的影响,本试验通过采集成年牦牛卵巢内颗粒细胞,分离培养后将其分为4个处理组,分别转染miR-96模拟物(mimics)和抑制物(inhibitor)及两者的阴性对照(NC)后培养并检测颗粒细胞受到的影响。使用流式细胞术和CCK-8法对细胞凋亡和增殖情况进行检测,采用qPCR和Western Blot检测凋亡相关基因表达情况,ELISA检测转染后类固醇激素分泌情况。结果表明：miR-96-mimics使颗粒细胞凋亡发生抑制促进细胞增殖,并促使凋亡相关基因Bcl-2表达极显著升高,Bax表达极显著降低;ELISA检测类固醇激素水平变化显示,与mimics NC组相比miR-96-mimics组细胞培养液中孕酮(P4)分泌水平极显著降低,雌二醇(E₂)分泌水平极显著升高;与inhibitor NC组相比miR-96-inhibitor组孕酮(P4)分泌水平极显著升高,雌二醇(E₂)分泌水平显著降低。miR-96可促进颗粒细胞增殖并抑制凋亡,同时会对生殖激素分泌产生影响,从而参与调控牦牛卵...     

对映-贝壳杉烷二萜化合物Wangzaozin A对人胃腺癌细胞SGC-7901生长的影响

利用形态观察法、台盼蓝排染法、集落形成法及姬姆萨染色法研究了从甘肃产拟缺香茶菜(Isodon excisoides(Sun ex C.H.Hu)C.Y.Wu et H.W.Li)中分离得到的二萜化合物Wangzaozin A对人胃腺癌细胞SGC-7901的增殖抑制作用及致死效应.结果表明,二萜化合物Wangzaozin A对SGC-7901细胞的生长状况有显著影响,具体表现为低浓度(≤4μmol.L-1)条件下抑制细胞增殖,高浓度(≥8μmol.L-1)条件下致细胞死亡,且具有时间-剂量依赖效应;姬姆萨染色显示,在高浓度条件下,Wangzaozin A能诱导人胃腺癌细胞SGC-7901发生凋亡.     

奥沙利铂黄芩素联合应用对胃癌细胞抑制作用的影响研究

目的观察奥沙利铂与黄芩素联用对人胃癌细胞株SGC-7901的抑制作用.方法实验分为对照组、给药组(奥沙利铂组、黄芩素组、联合作用组).应用MTT法测定给药组不同给药浓度对胃癌SGC-7901细胞株增殖的影响;倒置显微镜下观察对照组、给药组培养48 h后的细胞形态学变化;应用流式细胞术检测对照组、给药组胃癌SGC-7901细胞株凋亡率;HOE33258染色观察细胞凋亡形态学改变.结果奥沙利铂组、黄芩素组、联合作用组均可有效抑制SGC-7901细胞增殖,呈明显的量效关系;其中联合作用组抑制率明显高于奥沙利铂组和黄芩素组,差异具有显著统计学意义(P0.01).奥沙利铂组、黄芩素组SGC-7901细胞凋亡率明显高于对照组,差异具有显著统计学意义(P0.05).联合作用组细胞凋亡率明显高于对照组、奥沙利铂组、黄芩素组,差异具有显著统计学意义(P0.05).结论奥沙利铂与黄芩素联用可显著抑制人胃癌细胞株SGC-7901细胞增殖,诱导细胞凋亡.     

长链非编码RNA LINC00478抑制微小RNA-214对口腔鳞癌细胞顺铂耐药性的影响

目的:探讨长链非编码RNA LINC00478对口腔鳞癌细胞顺铂耐药性的影响及其对微小RNA-214(miR-214)的靶向调控作用.方法:采用qRT-PCR法检测口腔鳞癌组织、癌旁组织中LINC00478、miR-214的表达量;体外培养口腔鳞癌细胞CAL-27,建立顺铂耐药性细胞CAL-27/DDP,分别将pcDN...     

大蒜素对肺腺癌细胞侵袭生物学行为影响的初步研究

通过MTT法、细胞粘附试验、Transwell细胞迁移和侵袭试验检测不同浓度的大蒜素对肺腺癌细胞的活性、粘附、迁移与侵袭能力的变化;(RT-qPCR)逆转录-定量聚合酶链反应检测不同浓度的大蒜素对TIMP/MMP平衡的影响.本研究中发现大蒜素可呈剂量依赖性抑制肺腺癌细胞的活性、粘附、迁移和侵袭能力.大蒜素主要降低基质金...     

酶联免疫吸附测定法检测苏云金杆菌187菌株晶体蛋白的研究

本文采用液体双相法分离苏云金杆菌以色变种187菌株产生的伴孢晶体,然后碱解提取具体物活性的晶体毒素蛋白作为抗原,以ELISA间接法测定,最低检测阀值为1ng/ml。最敏感的检测区间为10~(-6)—10~(-9)g/ml。此区间内,抗原浓度的负对数值与ELISA的吸光值呈直线关系,其直线回归方程为(?)=6.457-0.3x。     

Amplification of the miR-181c/d cluster is inversely correlated with PDCD4 expression in gastric cancer

miR-181c/d is dysregulated in gastric cancer （GC）. We investigated the amplification and expression of miR-181c/d and its predicted target genes in GC. Amplification of miR-181c/d was quantified by genomic real-time PCR in GC and adjacent normal tissues, as well as the levels of mature miR-181c/d was performed by real-time PCR in the same tissues. The potential target genes of miR-181c/d were predicted using bioinformatics software. Expression of one potential target gene, PDCD4, was measured by semiquantitative RT-PCR, real-time PCR, and immunohistochemistry. Next, the relationship between miR181c/d expression and PDCD4 expression was analyzed. Results indicated that the amplification and expression of miR-181 c/d were significantly higher in GC than in adjacent normal tissues （primary miR-181 c/d, P 〈 0.001; miR-181 c,P = 0.0344; miR-18 ld, P = 0.0153）, and there was a strong correlation between mature miR-181c/d and primary miR-181c/d. Thirty-two target genes were predicted, including PDCD4 which is a known tumor suppressor gene. Expression of PDCD4 was significantly down-regulated in GC as compared to adjacent normal tissues and was inversely correlated with miR-181c/d expression in GC （miR-18lc and PDCD4： R = -0.496, P = 0.008; miR-181d and PDCD4： R = -0.454, P = 0.003）. Therefore, miR-181c/d may play a pivotal role in the pathogenesis of GC by down- regulating PDCD4 expression.     

家族性和三阴性乳腺癌血清中miR-21的表达

目的:检测血清miR-21在乳腺癌中的表达差异,为进一步阐明miR-21在家族性和三阴性乳腺癌发病机制中的作用.方法:收集健康女性体检者、具有患乳腺癌高风险者、不同种类乳腺癌患者的血清.以线虫miR-39为外参,通过实时荧光定量PCR检测77份血清中miR-21的表达水平.结果:家族性乳腺癌组、三阴性乳腺癌组和乳腺癌高风险组血清miR-21水平显著高于正常对照组、其他乳腺癌组(P0.01).血清miR-21的表达水平与淋巴结转移、Ki67高表达有关(P0.01).结果显示血清miR-21表达量在家族性和三阴性乳腺癌中升高,且与淋巴结转移和Ki67表达有关.结论:血清miR-21与三阴性、家族性乳腺癌的发生有紧密联系,其表达增高与乳腺癌的遗传性、恶性程度及预后判断有关.     

Recombinant soluble TRAIL induces apoptosis of cancer cells

TRAIL is a tumor necrosis factor family member that selectively induces apoptosis of cancer cells but not of normal cells. To develop TRAIL into a potential cancer drug, three different sizes of soluble TRAIL fragments, including sTRAIL(74—281), sTRAIL(95—281) and sTRAIL(101—281), were expressed in E. coli and purified to homogeneity. Apoptosis assays indicated that sTRAIL(95—281) and sTRAIL(101—281), but not sTRAIL(74—281), can potently induce apoptosis of various cancer cell lines in 6 h, suggesting that the N-terminal fragment of aa101 has inhibitory effect on TRAIL-induced apoptosis. Moreover, we found that some cancer cells were resistant to TRAIL and the resistant cells could be converted into sensitive cells by treatment with the protein synthesis inhibitor cycloheximide, suggesting that one or more short-lived proteins are responsible for cells’ resistance to TRAIL.     

替吉奥联合奥沙利铂治疗晚期胃癌的近期疗效观察

目的观察替吉奥联合奥沙利铂治疗晚期胃癌的近期疗效和不良反应。方法选取36例晚期胃癌患者,替吉奥胶囊80mg/m^2,分2次在早晚饭后半小时用水吞服,连续服用14天停7天,21天为1疗程。第1天奥沙利铂注射液130mg／m^2避光缓慢滴注2h-4h。连续治疗2个疗程后评价疗效。结果总有效率为52．8％（19／36）,临床收益率为81．6％（29／36）;主要不良反应为消化道反应、骨髓抑制,且多绝大多数为I-Ⅱ度。结论替吉奥联合奥沙利铂治疗晚期胃癌近期疗效较好,不良反应可以耐受。     

替吉奥联合多西他赛方案治疗进展期胃癌的临床观察

目的观察替吉奥联合多西他赛治疗进展期胃癌的近期疗效和毒副反应。方法44例进展期胃癌患者采用以下方法化疗：替吉奥胶囊每天80mg／m^2,分2次,餐后口服,第1-14天;多西他赛75mg／m^2,第1天,静脉滴注2-3h,21d为1个周期,至少完成2个周期。评价客观疗效和不良反应。结果44例均可以评价疗效。CR3例（6．8％）,PR18例（40．9％）,SD14例（31．8％）,PD9例（20．5％）,RR47．7％,DCR79．5％。中位疾病进展时间为7．2月,中位生存期为11．3月。不良反应主要是骨髓抑制、胃肠道反应、脱发及口腔黏膜炎。结论替吉奥联合多西他赛方案治疗进展期胃癌的疗效较好,不良反应可以耐受,值得进一步研究应用。     

灯盏乙素对乳腺癌细胞中lncRNAs表达的影响

检测灯盏乙素对乳腺癌MDA-MB-231细胞中的长链非编码RNA(LncRNAs)的相对表达量的影响,进一步探索灯盏乙素对肿瘤的作用机制.采用实时荧光定量PCR的方法,检测对照组与不同剂量组的灯盏乙素处理后的乳腺肿瘤细胞中lncRNAs MALAT1、NEAT1和p53基因mRNA的相对表达量,并观察细胞存活率.结果发现,灯盏乙素在低剂量(1、10、25μmol/L)时促进细胞增殖,而在高剂量50μmol/L以上时抑制细胞增殖.灯盏乙素在低剂量时使得乳腺癌MDA-MB-231细胞中MALAT1,NEAT1和p53基因的表达水平下降,而在100μmol/L的高剂量时MALAT1,NEAT1和p53基因的表达水平上升.灯盏乙素影响乳腺癌MDA-MB-231细胞中LncRNAs MALAT1和NEAT1基因以及p53基因的表达,并且存在剂量反应关系,低剂量与高剂量呈现出相反的表达量变化.     

新型多酸化合物对人乳腺癌细胞增殖的抑制作用

采用MTT法、形态学方法和Western blot方法,检测了3种新型多酸化合物[SbW9、（SbW9）2-（SnR）4、（SbW9）2-（SnR-CH3）4]对人乳腺癌MCF7和MDA-MB-231细胞生长抑制作用,细胞形态学变化及细胞PCNA蛋白表达变化,并探讨该3种化合物抑癌的机制.实验结果表明：3种化合物对人乳腺癌细胞MCF7和MDA-MB-231的生长均具有明显的抑制作用（P〈0.01）,细胞形态发生明显变化,细胞皱缩并且增殖速度明显减慢;其中,（SbW9）2-（SnR）4可使MCF7细胞PCNA蛋白表达下降（P〈0.05）,且呈浓度剂量依赖性.说明该3种新型多酸化合物均具有抗肿瘤活性,其活性部位可能是以{SbW9}为基本建筑单元的聚阴离子,作用机制可能与其抑制细胞DNA的合成有关.     

The application of Tau protein testing to gastric cancer patients treated with paclitaxel

Paclitaxel is one of the main drugs used to treat gastric cancer, but many tumors develop drug resistance, resulting in treatment failure. The levels of expression of Tan protein in breast tumors have been found to be related to paclitaxel resistance, suggesting that Tau protein expression may predict breast cancer sensitivity to paclitaxel treatment. To determine whether Tan protein ex- pression can predict gastric cancer sensitivity to paclitaxel, we assayed Tan protein expression levels in gastric cancer specimens from 70 patients. We observed Tan protein expression in 54 of 70 （77.1%） specimens. Assays in gastric cancer cell lines showed that Tan protein expression was significantly lower in BGC823 than in MKN45 cells （P -- 0.0147）. MTT assays showed that dif- ferent concentrations of paclitaxel inhibited the growth of MKN45 and BGC823 cells, but inhibition and apoptosis were more obvious in cells expressing low levels of Tau protein. Paclitaxel chemotherapy was effective in 34 of the 70 patients （48.6%） and was significantly correlated with low expression of Tau protein （P 〈 0.01）. These findings indicate that Tau protein is expressed in a high percentage of gastric cancers, with paclitaxel being more effective in tumors with low Tau expression.