胃癌细胞TRAIL受体的表达与其对TRAIL敏感性的关系

目的:探讨胃癌细胞表面TRAIL受体表达水平及其与TRAIL敏感性的关系.方法:PI染色、流式细胞仪检测TRAIL诱导BGC-823及SGC-7901细胞的凋亡率,流式细胞仪检测细胞膜表面四种TRAIL受体-R1、R2、R3、R4的表达情况.结果:TRAIL诱导胃癌细胞凋亡具有剂量和时间依赖性,BGC-823较SGC-7901对TRAIL诱导的凋亡更敏感,TRAIL(100μg·L-1)作用24h的细胞凋亡率分别是59.9%、24.3%.死亡受体TRAIL-R1/DR4、TRAIL-R2/DR5在BGC-823细胞膜表面表达的阳性率高达97.87%和99.42%,而在SGC-7901分别为7.03%和95-31%,诱骗受体TRAIL-R3/DcR1、TRAIL-R4/DcR2在两株细胞膜表面极少表达.结论:胃癌细胞对TRAIL诱导凋亡的敏感性差异可能与细胞膜表面死亡受体有关,尤其与DR4的表达有关.     

Following a TRAIL： Update on a ligand and its five receptors

Identification of tumour necrosis factor apoptosis inducing ligand (TRAIL), a TNF family ligand, sparked a torrent of research, following an initial observation that it could kill tumour cells, but spare normal cells. Almost a decade after its discovery, and with five known receptors, the true physiological role of TRAIL is still debated and its anti-tumorigenic properties limited by potential toxicity. This review takes a comprehensive look at the story of this enigmatic ligand,addressing its remaining potential as a therapeutic and providing an overview of the TRAIL receptors themselves.     

反义bcl—2在胃癌细胞中的诱导表达及促凋亡作用

为了观察ｂｃｌ－２反义ＲＮＡ对胃癌细胞ＳＧＣ７９０１的促凋亡作用及ＭＴ－１１启动子的启动诱导活性,用分子克隆方法构建载体,以电泳术,电镜术,流式细胞术,原位杂交,裸鼠肿瘤抑制试验及化学发光分析等方法观察,结果表明,可诱导载体ｐＭＴｂＮ具有良好的诱导启动转录活性,Ｂｃｌ－２蛋白的表达下降使胃癌细胞ＳＧＣ７９０１更易发生凋亡,致瘤性也发生改变。     

Bcl—2的抗细胞凋亡机制

Ｂｃｌ－２的抗细胞凋亡机制＠郑英如＠陈竹钦￥第三军医大学附属大坪医院Ｂｃｌ２的抗细胞凋亡机制郑英如陈竹钦（第三军医大学附属大坪医院，重庆６３００４２）ｂｃｌ２为一原癌基因，通过其所编码蛋白Ｂｃｌ２而发挥其抑制细胞凋亡的功能。在生理情况下，Ｂｃｌ２在...     

TRAIL联合多西紫杉醇诱导喉鳞癌Hep-2 细胞凋亡的实验研究

目的：观察肿瘤坏死因子相关凋亡诱导配体( TRAIL) 联合多西紫杉醇应用于人喉鳞癌Hep-2 细胞生长的抑制增殖和诱导 凋亡作用。方法：实验分四组,1 组对照组,2 组为应用TRAIL组,3 组单独应用多西紫杉醇,4 组联合应用TRAIL及多西紫杉醇。 分别应用MTT、流式细胞仪检测细胞凋亡率,倒置显微镜观察细胞的形态学改变。结果：TRAIL 与多西紫杉醇联合作用于Hep-2 细胞,能显著增强对Hep-2 细胞的杀伤、抑制增殖及诱导凋亡作用,其联合应用的凋亡抑制率明显高于单独应用TRAIL组和多西 紫杉醇组( P<0.05)。结论：TRAIL与多西紫杉醇联用能显著提高对喉鳞癌Hep-2 细胞的生长抑制和诱导凋亡作用。     

TRAIL联合多西紫杉醇诱导喉鳞癌Hep-2细胞凋亡的实验研究

目的：观察肿瘤坏死因子相关凋亡诱导配体（TRAIL）联合多西紫杉醇应用于人喉鳞癌Hep-2细胞生长的抑制增殖和诱导凋亡作用。方法：实验分四组,1组对照组,2组为应用TRAIL组,3组单独应用多西紫杉醇,4组联合应用TRAIL及多西紫杉醇。分别应用MTT、流式细胞仪检测细胞凋亡率,倒置显微镜观察细胞的形态学改变。结果：TRAIL与多西紫杉醇联合作用于Hep-2细胞,能显著增强对Hep-2细胞的杀伤、抑制增殖及诱导凋亡作用,其联合应用的凋亡抑制率明显高于单独应用TRAIL组和多西紫杉醇组（P〈0．05）。结论：TRAIL与多西紫杉醇联用能显著提高对喉鳞癌Hep-2细胞的生长抑制和诱导凋亡作用。     

Signal transduction mediated by Bid,a pro—death Bcl—2 family proteins,connects the death receptor and mitochondria apoptosis pathways

Two major apoptosis pathways have been defined in mammalian cells,the Fas/TNF-R1 death receptor pathway and the mitochondria pathway.The Bcl-2 family proteins consist of both anti-apoptosis and pro-apoptosis members that regulate apoptosis,mainly by controlling the release of cytochrome c and other mitochondrial apoptotic events.However,death signals mediated by Fas/TNF-R1 receptors can usually activate caspases directly,bypassing the need for mitochondria and escaping the regulation by Bcl-2 family proteins.Bid is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals.Activated Bid is translocated to mitochondria and induces cytochrome c release,which in turn activates downstream caspases.Such a connection between the two apoptosis pathways could be important for induction of apoptosis in certain types of cells and responsible for the pathogenesis of a number of human diseases.     

鼻咽癌Epstein—Barr病毒受体（EBVR／CR2）基因的病毒结合区的序列测定

Ｅｐｓｔｅｉｎ－Ｂａｒｒ病毒（ＥＢＶ）进入鼻咽上皮细胞的途径,是人们研究ＥＢＶ与鼻咽癌（ＮＰＣ）的病因关系时所必须回答的一个问题。用抗ＥＢＣ受体（ＥＢＶＲ／ＣＲ２）单抗检测上皮细胞中该受体的表达已有报道,但对上皮细胞中ＥＢＶＲ／ＣＲ２的基因结构仍需研究。我们采用ＰＣＲ扩增和不对称ＰＣＲ直接测序法,首次检测了１０例ＮＰＣ及３例正常人胚鼻咽上皮（Ｈｕｍａｎ ｅｍｂｒｙｏｎｉｃ ｎａｓｏｐｈａｒｙｎｇｅ     

肾细胞癌CD15和BCL—2的表达及临床意义

为了探讨评估肾细胞癌（RCC）预后指标,应用免疫组化法研究60例RCC中细胞粘附分子CD15和Bcl-2蛋白表达及其相关关系。结果表明,在RCC中CD15和Bcl-2表达阳性率分别为70.0%和61.7%。CD15高表达与RCC分级、分期和淋巴结转移有关。Bcl-2低表达与RCC分级有关,与其分期和淋巴结转移无关。CD15表达与Bcl-2表达呈负相关。结果提示,CD15表达是RCC发生、发展和转移的指标,Bcl-2是RCC发生的早期事件。     

ATM和ATR：在G2—M期阻滞与凋亡中的作用及相互关系

ATR和ATM是DNA损伤引起的G2—M期阻滞的主要信号因子,它们通过调节不同的细胞因子在细胞G2—M期阻滞中发挥不同的作用,并且它们相互作用在诱发细胞凋亡方面也有重要意义。本文着重阐述了近年来报道的有关ATR和ATM在G2—M期阻滞与凋亡中的作用及相互关系方面的研究进展。     

HeLa细胞中hR24L基因的表达、DNA损伤修复、G2／M阻滞与电离辐射之间的关系（简报）

The hR24L gene ORF was cloned from the total RNA of HeLa cells by RT-PCR method. There is no mutation of the hR24L gene in HeLa cells. Ion radiation significantly increased the expression of hR24L gene, and the sense hR24L enhanced and accelerated the cell cycle arrest at G2/M phase in HeLa cells. Besides, it should seem that the overexpression of hR24L gene could enhance the repair ability of DNA damage induced by ion radiation, and vice versa.