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首页> 外文期刊>Journal of cellular biochemistry. >Effect of hyperthermia and chemotherapeutic agents on TRAIL-induced cell death in human colon cancer cells.
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Effect of hyperthermia and chemotherapeutic agents on TRAIL-induced cell death in human colon cancer cells.

机译：高温和化学治疗剂对TRAIL诱导的人结肠癌细胞死亡的影响。

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摘要

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising cancer therapeutic agent because of its tumor selectivity. TRAIL is known to induce apoptosis in cancer cells but spare most normal cells. In the previous study [Yoo and Lee, 2007], we have reported that hyperthermia could enhance the cytotoxicity of TRAIL-induced apoptosis. We observed in human colorectal cancer cell line CX-1 that TRAIL-induced apoptotic death and also that mild hyperthermia promoted TRAIL-induced apoptotic death through caspase activation and cytochrome-c release. Although its effects in vivo are not clear, hyperthermia has been used as an adjunctive therapy for cancer. Hyperthermia is often accompanied by chemotherapy to enhance its effect. In this study, CX-1 colorectal adenocarcinoma cells were treated with TRAIL concurrently with hyperthermia and oxaliplatin or melphalan. To evaluate the cell death effects on tumor cells via hyperthermia and TRAIL and chemotherapeutic agents, FACS analysis, DNA fragmentation, and immunoblottings for PARP-1 and several caspases and antiapoptotic proteins were performed. Activities of casapse-8, caspase-9, and caspase-3 were also measured in hyperthermic condition. Interestingly, when analyzed with Western blot, we detected little change in the intracellular levels of proteins related to apoptosis. Clonogenic assay shows, however, that chemotherapeutic agents will trigger cancer cell death, either apoptotic or non-apoptotic, more efficiently. We demonstrate here that CX-1 cells exposed to 42 degrees C and chemotherapeutic agents were sensitized and died by apoptotic and non-apoptotic cell death even in low concentration (10 ng/ml) of TRAIL.
机译：肿瘤坏死因子相关的凋亡诱导配体（TRAIL）由于其肿瘤选择性是一种有前途的癌症治疗剂。众所周知，TRAIL会诱导癌细胞凋亡，但会保留大多数正常细胞。在先前的研究中[Yoo and Lee，2007]，我们已经报道了高温可以增强TRAIL诱导的细胞凋亡的细胞毒性。我们在人结肠直肠癌细胞系CX-1中观察到TRAIL诱导的细胞凋亡死亡，并且温和的高温通过胱天蛋白酶激活和细胞色素C释放促进TRAIL诱导的细胞凋亡死亡。尽管尚不清楚其在体内的作用，但高温疗法已被用作癌症的辅助疗法。热疗经常伴随化学疗法以增强其效果。在这项研究中，TRAIL联合高热和奥沙利铂或美法仑治疗CX-1大肠腺癌细胞。为了评估通过热疗和TRAIL及化学治疗剂对肿瘤细胞的细胞死亡效应，进行了FACS分析，DNA片段化和PARP-1以及几种半胱氨酸蛋白酶和抗凋亡蛋白的免疫印迹。在高温条件下也测定了casapse-8，caspase-9和caspase-3的活性。有趣的是，当用蛋白质印迹分析时，我们发现细胞内与凋亡相关的蛋白质水平几乎没有变化。然而，克隆形成试验表明，化学治疗剂将更有效地触发凋亡或非凋亡的癌细胞死亡。我们在这里证明，即使在低浓度（10 ng / ml）的TRAIL中，暴露于42度C和化学治疗剂的CX-1细胞也会被凋亡和非凋亡细胞致敏并死亡。

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