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单胺氧化酶 A 在 HPV-16 E7 诱导的非小细胞肺癌细胞上皮-间充质转化和 HIF-1α 蛋白积累中的作用。

The role of monoamine oxidase A in HPV-16 E7-induced epithelial-mesenchymal transition and HIF-1α protein accumulation in non-small cell lung cancer cells.

机构信息

Institute of Biochemistry and Molecular Biology, Collaborative innovation center for antitumor active substance research and development, Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Guangdong Medical University, Zhanjiang 524023, P.R. China.

Marine Medical Research Institute of Guangdong Zhanjiang, Guangdong Key Laboratory for Research and Development of Natural Drugs, Guangdong Medical University, Zhanjiang 524023, P.R. China.

出版信息

Int J Biol Sci. 2020 Aug 1;16(14):2692-2703. doi: 10.7150/ijbs.46966. eCollection 2020.

DOI:10.7150/ijbs.46966
PMID:32792865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7415426/
Abstract

Our previous studies have found that human papillomavirus (HPV)-16 E7 oncoprotein promotes epithelial-mesenchymal transition (EMT) and hypoxia-inducible factor-1α (HIF-1α) protein accumulation in non-small cell lung cancer (NSCLC) cells and monoamine oxidase A (MAOA) is highly expressed in NSCLC tissues. Here, we further explored the role of MAOA in HPV-16 E7-induced EMT and HIF-1α protein accumulation in A549 and NCI-H460 NSCLC cells. Our results showed that HPV-16 E7 enhanced MAOA expression in NSCLC cells. Additionally, MAOA knockout inhibited HPV-16 E7-induced migration, invasion, and EMT, and significantly reduced HPV-16 E7-induced ROS generation and HIF-1α protein accumulation promoting its degradation. Furthermore, MAOA knockout suppressed HPV-16 E7-induced ERK1/2 activation. , MAOA knockout inhibited tumor growth, metastasis, and the expression of EMT-related markers and HIF-1α proteins induced by HPV-16 E7 in NCI-H460 NSCLC subcutaneous xenograft and intrapulmonary models of nude mice. Taken together, our findings provide evidence that MAOA plays a key role in EMT and HIF-1α protein accumulation induced by HPV-16 E7 in NSCLC cells, suggesting that MAOA may be a potential therapeutic target for HPV-related NSCLC.

摘要

我们之前的研究发现，人乳头瘤病毒（HPV）-16 E7 癌蛋白促进非小细胞肺癌（NSCLC）细胞中的上皮-间充质转化（EMT）和缺氧诱导因子-1α（HIF-1α）蛋白积累，而单胺氧化酶 A（MAOA）在 NSCLC 组织中高度表达。在这里，我们进一步探讨了 MAOA 在 HPV-16 E7 诱导的 EMT 和 HIF-1α 蛋白积累中的作用，在 A549 和 NCI-H460 NSCLC 细胞中进行了研究。我们的结果表明，HPV-16 E7 增强了 NSCLC 细胞中的 MAOA 表达。此外，MAOA 敲除抑制了 HPV-16 E7 诱导的迁移、侵袭和 EMT，并显著减少了 HPV-16 E7 诱导的 ROS 生成和 HIF-1α 蛋白积累，促进其降解。此外，MAOA 敲除抑制了 HPV-16 E7 诱导的 ERK1/2 激活。MAOA 敲除抑制了 NCI-H460 NSCLC 皮下移植瘤和裸鼠肺内模型中 HPV-16 E7 诱导的肿瘤生长、转移以及 EMT 相关标志物和 HIF-1α 蛋白的表达。综上所述，我们的研究结果表明，MAOA 在 HPV-16 E7 诱导的 NSCLC 细胞 EMT 和 HIF-1α 蛋白积累中发挥关键作用，提示 MAOA 可能是 HPV 相关 NSCLC 的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a8e/7415426/d19aef17cae1/ijbsv16p2692g007.jpg
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