Caspase- and p38-MAPK-dependent induction of apoptosis in A549 lung cancer cells by Newcastle disease virus
Caspase- and p38-MAPK-dependent induction of apoptosis in A549 lung cancer cells by Newcastle disease virus
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DOI：
10.1007/s00705-011-0987-y
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发表时间：
2011-08-01
影响因子：
2.7
通讯作者：
Meng, Songshu
中科院分区：
文献类型：
--
作者：
Bian, Jianchun;Wang, Kai;Meng, Songshu
纽卡斯尔病病毒（NDV）能诱导肿瘤细胞凋亡，具有潜在的溶瘤作用。然而，以往的研究表明，关于NDV诱导的肿瘤细胞凋亡信号通路的差异。在这里，我们表明，NDV感染诱导A549人肺癌细胞的内在和外在死亡途径的同时激活。与此相反，内质网（ER）的压力是不激活NDV诱导的细胞凋亡。我们首次证明了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，我们的发现为NDV诱导肿瘤细胞凋亡的潜在机制提供了新的见解。
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.