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首页> 外文期刊>Archives of Toxicology >Mitogen-activated protein kinases mediate arsenic-induced down-regulation of survivin in human lung adenocarcinoma cells.
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Mitogen-activated protein kinases mediate arsenic-induced down-regulation of survivin in human lung adenocarcinoma cells.

机译：丝裂原激活的蛋白激酶介导砷诱导的人肺腺癌细胞中survivin的下调。

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摘要

Survivin is a member of the inhibitors of apoptosis protein (IAP) family and is highly expressed in various cancer cells. However, the molecular mechanisms regulating survivin expression remain unclear. In this study, we investigated the role of mitogen-activated protein kinases (MAPKs) in regulating survivin in the human lung adenocarcinoma cell line H1355 in response to arsenic trioxide (As(3+)). Our data indicated that As(3+) induced cytotoxicity accompanied by down-regulation of survivin, cleavage of Poly ADP-ribosyl polymerase (PARP) and activations of MAPKs, including ERK1/2, p38 and c-jun N-terminal kinase (JNK). We found that blockage of p38 or JNK activation attenuated the As(3+)-induced survivin down-regulation and PARP cleavage with significant reversal of cell viability, however, by only 5-8%. On the other hand, the MEK inhibitor PD098059 or the ubiquitin-proteasome inhibitor MG-132 exhibited little effect on survivin down-regulation and PARP cleavage induced by As(3+). In this study, we demonstrated that As(3+) could down-regulate survivin via activations of p38 and JNK in an ubiquitin-proteasome independent pathway and lead to cytotoxicity and apoptosis in the human lung adenocarcinoma cell line H1355.
机译：Survivin是凋亡蛋白（IAP）抑制剂家族的成员，并在各种癌细胞中高度表达。但是，尚不清楚调节生存素表达的分子机制。在这项研究中，我们调查了有丝分裂原激活的蛋白激酶（MAPKs）在调节人肺腺癌细胞H1355对三氧化二砷（As（3+））的存活蛋白中的作用。我们的数据表明，As（3+）诱导的细胞毒性伴随着survivin的下调，聚ADP-核糖基聚合酶（PARP）的裂解和MAPK的激活，包括ERK1 / 2，p38和c-jun N末端激酶（JNK ）。我们发现，p38或JNK激活的阻滞减弱了As（3+）诱导的survivin下调和PARP裂解，但细胞活力却发生了显着逆转，仅降低了5-8％。另一方面，MEK抑制剂PD098059或泛素-蛋白酶体抑制剂MG-132对As（3+）诱导的survivin下调和PARP裂解作用不大。在这项研究中，我们证明了As（3+）可以通过泛素-蛋白酶体独立途径中p38和JNK的激活来下调survivin，并导致人肺腺癌细胞H1355的细胞毒性和凋亡。

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