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首页> 外文会议>International Conference on Bioinformatics and Biomedical Engineering >Endoplasmic reticulum stress signaling pathways is involved in trichosanthin-induced apoptosis in human cervical cancer cell line Hela
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Endoplasmic reticulum stress signaling pathways is involved in trichosanthin-induced apoptosis in human cervical cancer cell line Hela

机译：内质网胁迫信号传导途径涉及人宫颈癌细胞系Hela中的Trichosanthin诱导的细胞凋亡

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Endoplasmic reticulum stress(ERS)is a kind of subcellular pathological process which result from calcium disorderliness and protein improper folding. And endoplasmic reticulum stress induced apoptosis is a novel pathway which different from the mitochondria-initiated intrinsic pathway and the death receptor-triggered extrinsic pathway. Trichosanthin (TCS), a type I ribosome-inactivating protein, induces cell death in various cell types including several tumor cell lines. However, the mechanism remains largely uncharacterized. The aim of present study is to explore possible mechanism underlying its cytotoxicity by using human cervical cancer Hela cell line as a model. We found that TCS induced apoptosis in Hela cells in a time- and dose- dependent manner. cDNA microarray analysis demonstrated that there were 62 pieces of gene up-regulated and 16 pieces of gene down-regulated after treated with TCS, subsequent analysis by RT-PCR and western blot confirmed that GRP78 and calpain could be significantly induced by TCS, which strongly supported the involvement of endoplasmic reticulum stress pathway in TCS-induced apoptosis. This study reveals a new pathway of endoplamic reticulum stress in TCS induces apoptosis in hela cells, Further research with more cell lines and calpain inhibitor needs to be performed to determine if calpian activation is a common feature in TCS-induced apoptosis.
机译：内质网胁迫（ERS）是一种亚细胞病理过程，由钙紊乱和蛋白质不当折叠产生。内质网胁迫诱导的细胞凋亡是一种新的途径，其不同于线粒体引发的内在途径和死亡受体触发的外在途径。 Trichosanthin（TCS），I型核糖体灭活蛋白，诱导包括几种肿瘤细胞系的各种细胞类型的细胞死亡。然而，该机制仍然大大不具表明。目前研究的目的是通过使用人宫颈癌Hela细胞系作为模型来探讨其细胞毒性下面的可能机制。我们发现TCS以时间和剂量依赖性的方式在HeLa细胞中诱导细胞凋亡。 cDNA微阵列分析证明，用TCS处理过62个基因上调和16个基因下调，随后通过RT-PCR和Western印迹分析，确认GRP78和CALPAIN可以由TCS显着诱导，强烈支持在TCS诱导的细胞凋亡中的内质网应激途径参与。本研究揭示了TCS中的先前型网状胁迫的新途径在HeLa细胞中诱导细胞凋亡，需要进行更多细胞系和钙骨抑制剂的研究以确定CALPIAN活化是TCS诱导的细胞凋亡中的常见特征。

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