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P38MAPK 与自噬的串扰对 Fas 抗体/放线菌素 D 诱导人肝癌 Bel-7402 细胞中线粒体介导的凋亡的影响。

Crosstalk Influence between P38MAPK and Autophagy on Mitochondria-Mediated Apoptosis Induced by Anti-Fas Antibody/Actinomycin D in Human Hepatoma Bel-7402 Cells.

机构信息

Basic Medicine Department, Qiqihar Medical University, Qiqihar 161006, China.

Pharmacy Department, Qiqihar Medical University, Qiqihar 161006, China.

出版信息

Molecules. 2017 Oct 17;22(10):1705. doi: 10.3390/molecules22101705.

DOI:10.3390/molecules22101705
PMID:29039784
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6151482/
Abstract

Our previous study indicated that anti-Fas antibody/actinomycin D (AF/AD) induced apoptosis of human hepatocellular carcinoma Bel-7402 cells; however, crosstalk influence between P38MAPK and autophagy on mitochondria-mediated apoptosis induced by AF/AD in Bel-7402 cells remains unclear. Therefore, effect of AF/AD on apoptosis, autophagy, phosphorylated-P38MAPK (p-P38MAPK), and membrane potential (ΔΨm) with or without the P38MAPK inhibitor SB203580 or the autophagy inhibitor 3-methyladenine (3-MA) in Bel-7402 cells was investigated in the present study. The results showed that AF/AD resulted in induction of apoptosis concomitant with autophagy, upregulation of p-P38MAPK and autophagy-associated gene proteins (Atg5-Atg12 protein complex, Atg7, Atg10, Beclin-1, LC3 I, and LC3 II), and downregulation of ΔΨm in Bel-7402 cells. In contrast, SB203580 attenuated the effects of AF/AD in Bel-7402 cells. Furthermore, the findings also demonstrated that 3-MA inhibited the impact of AF/AD on autophagy, Atg5-Atg12 protein complex, Atg7, Atg10, Beclin-1, LC3 I, LC3 II, and ΔΨm, and promoted the influence of AF/AD on apoptosis and p-P38MAPK in Bel-7402 cells. Taken together, we conclude that crosstalk between P38MAPK and autophagy regulates mitochondria-mediated apoptosis induced by AF/AD in Bel-7402 cells.

摘要

我们之前的研究表明，抗 Fas 抗体/放线菌素 D（AF/AD）诱导人肝癌 Bel-7402 细胞凋亡；然而，AF/AD 诱导 Bel-7402 细胞中线粒体介导的凋亡过程中 P38MAPK 和自噬之间的串扰影响尚不清楚。因此，本研究探讨了 AF/AD 对 Bel-7402 细胞凋亡、自噬、磷酸化-P38MAPK（p-P38MAPK）和膜电位（ΔΨm）的影响，以及 P38MAPK 抑制剂 SB203580 或自噬抑制剂 3-甲基腺嘌呤（3-MA）对 AF/AD 的影响。结果表明，AF/AD 诱导 Bel-7402 细胞凋亡伴自噬，上调 p-P38MAPK 和自噬相关基因蛋白（Atg5-Atg12 蛋白复合物、Atg7、Atg10、Beclin-1、LC3 I 和 LC3 II），下调 Bel-7402 细胞的ΔΨm。相反，SB203580 减弱了 AF/AD 在 Bel-7402 细胞中的作用。此外，研究结果还表明，3-MA 抑制了 AF/AD 对自噬、Atg5-Atg12 蛋白复合物、Atg7、Atg10、Beclin-1、LC3 I、LC3 II 和ΔΨm 的影响，并促进了 AF/AD 对凋亡和 p-P38MAPK 的影响。综上所述，我们得出结论，P38MAPK 和自噬之间的串扰调节了 AF/AD 诱导的 Bel-7402 细胞中线粒体介导的凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/6151482/cfce43a5e33b/molecules-22-01705-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/6151482/74585803359e/molecules-22-01705-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/6151482/cfce43a5e33b/molecules-22-01705-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/6151482/74585803359e/molecules-22-01705-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/6151482/2b432baea08c/molecules-22-01705-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43e4/6151482/cfce43a5e33b/molecules-22-01705-g005a.jpg

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