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新城疫病毒诱导 A549 肺癌细胞凋亡的 Caspase 和 p38-MAPK 依赖性。

Caspase- and p38-MAPK-dependent induction of apoptosis in A549 lung cancer cells by Newcastle disease virus.

机构信息

National Key Laboratory of Veterinary Biotechnology, Chinese Academy of Agricultural Sciences, Harbin, 150001, Heilongjiang, China.

出版信息

Arch Virol. 2011 Aug;156(8):1335-44. doi: 10.1007/s00705-011-0987-y. Epub 2011 Apr 6.

DOI:10.1007/s00705-011-0987-y
PMID:21625975
Abstract

Newcastle disease virus (NDV) has a potential oncolytic effect due to its ability to induce apoptosis in tumor cells. However, previous studies have indicated discrepancies regarding the apoptosis signaling pathways induced by NDV in tumor cells. Here, we show that NDV infection induces simultaneous activation of intrinsic and extrinsic death pathways in A549 human lung cancer cells. In contrast, endoplasmic reticulum (ER) stress is not activated in NDV-induced apoptosis. We demonstrate for the first time that mitogen-activated protein kinase (MAPK) pathways are activated in NDV-infected A549 cells, and p38 MAPK is involved in NDV-induced cell death. Together, our findings provide novel insights into the underlying mechanisms by which NDV induces apoptosis in tumor cells.

摘要

新城疫病毒(NDV)由于能够诱导肿瘤细胞凋亡,具有潜在的溶瘤作用。然而,先前的研究表明,NDV 在肿瘤细胞中诱导凋亡的信号通路存在差异。在这里,我们表明 NDV 感染诱导 A549 人肺癌细胞中内在和外在死亡途径的同时激活。相比之下,NDV 诱导的细胞凋亡不会激活内质网(ER)应激。我们首次证明,丝裂原活化蛋白激酶(MAPK)途径在 NDV 感染的 A549 细胞中被激活,并且 p38 MAPK 参与 NDV 诱导的细胞死亡。总之,我们的研究结果为 NDV 诱导肿瘤细胞凋亡的潜在机制提供了新的见解。

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