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CLytA-DAAO 嵌合酶诱导人肿瘤细胞系细胞死亡的机制。

Cell Death Mechanisms Induced by CLytA-DAAO Chimeric Enzyme in Human Tumor Cell Lines.

机构信息

Unidad de Investigación, Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunidad Valenciana (FISABIO), Hospital General Universitario de Elche, Camí de l'Almazara, 11, 03203 Elche (Alicante), Spain.

Instituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE), Universidad Miguel Hernández, Avda. Universidad s/n, Ed. Torregaitán, 03202 Elche (Alicante), Spain.

出版信息

Int J Mol Sci. 2020 Nov 12;21(22):8522. doi: 10.3390/ijms21228522.

Abstract

The combination of the choline binding domain of the amidase N-acetylmuramoyl-L-alanine (CLytA)-D-amino acid oxidase (DAAO) (CLytA-DAAO) and D-Alanine induces cell death in several pancreatic and colorectal carcinoma and glioblastoma cell lines. In glioblastoma cell lines, CLytA-DAAO-induced cell death was inhibited by a pan-caspase inhibitor, suggesting a classical apoptotic cell death. Meanwhile, the cell death induced in pancreatic and colon carcinoma cell lines is some type of programmed necrosis. In this article, we studied the mechanisms that trigger CLytA-DAAO-induced cell death in pancreatic and colorectal carcinoma and glioblastoma cell lines and we acquire a further insight into the necrotic cell death induced in pancreatic and colorectal carcinoma cell lines. We have analyzed the intracellular calcium mobilization, mitochondrial membrane potential, PARP-1 participation and AIF translocation. Although the mitochondrial membrane depolarization plays a crucial role, our results suggest that CLytA-DAAO-induced cell death is context dependent. We have previously detected pancreatic and colorectal carcinoma cell lines (Hs766T and HT-29, respectively) that were resistant to CLytA-DAAO-induced cell death. In this study, we have examined the putative mechanism underlying the resistance in these cell lines, evaluating both detoxification mechanisms and the inflammatory and survival responses. Overall, our results provide a better understanding on the cell death mechanism induced by CLytA-DAAO, a promising therapy against cancer.

摘要

酰胺酶 N-乙酰胞壁酸-L-丙氨酸(CLytA)-D-氨基酸氧化酶(DAAO)的胆碱结合域(CLytA-DAAO)与 D-丙氨酸的结合诱导多种胰腺和结肠直肠癌细胞系和神经胶质瘤细胞系发生细胞死亡。在神经胶质瘤细胞系中,CLytA-DAAO 诱导的细胞死亡被一种广谱半胱天冬酶抑制剂所抑制,表明这是一种经典的细胞凋亡。同时,在胰腺和结肠直肠癌细胞系中诱导的细胞死亡是某种程序性坏死。在本文中,我们研究了触发 CLytA-DAAO 在胰腺和结肠直肠癌细胞系以及神经胶质瘤细胞系中诱导细胞死亡的机制,并进一步深入了解胰腺和结肠直肠癌细胞系中诱导的坏死性细胞死亡。我们分析了细胞内钙动员、线粒体膜电位、PARP-1 参与和 AIF 易位。尽管线粒体膜去极化起着至关重要的作用,但我们的结果表明,CLytA-DAAO 诱导的细胞死亡是上下文相关的。我们之前已经检测到对 CLytA-DAAO 诱导的细胞死亡具有抗性的胰腺和结肠直肠癌细胞系(分别为 Hs766T 和 HT-29)。在这项研究中,我们检查了这些细胞系中抗性的潜在机制,评估了解毒机制以及炎症和存活反应。总的来说,我们的研究结果为 CLytA-DAAO 诱导的细胞死亡机制提供了更好的理解,这是一种有前途的抗癌疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/741f/7697521/93aa7d7054a4/ijms-21-08522-g001.jpg

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