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雷公藤红素通过上调 microRNA-181a 抑制人神经母细胞瘤 SH-SY5Y 细胞的增殖和迁移。

Triptolide Inhibits Proliferation and Migration of Human Neuroblastoma SH-SY5Y Cells by Upregulating MicroRNA-181a.

机构信息

Department of Pediatrics, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, P.R. China.

Outpatient Department, Qingdao No. 1 Sanitarium, Qingdao, Shandong, P.R. China.

出版信息

Oncol Res. 2018 Sep 14;26(8):1235-1243. doi: 10.3727/096504018X15179661552702. Epub 2018 Feb 9.

DOI:10.3727/096504018X15179661552702
PMID:29426375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7844704/
Abstract

Neuroblastoma is the primary cause of cancer-related death for children 1 to 5 years of age. New therapeutic strategies and medicines are urgently needed. This study aimed to investigate the effects of triptolide (TPL), the major active component purified from Tripterygium wilfordii Hook F, on neuroblastoma SH-SY5Y cell proliferation, migration, and apoptosis, as well as underlying potential mechanisms. We found that TPL inhibited SH-SY5Y cell viability, proliferation, and migration, but induced cell apoptosis. The expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 after TPL treatment in SH-SY5Y cells was decreased. The expression of microRNA-181a (miR-181a) was upregulated after TPL treatment. Moreover, suppression of miR-181a reversed the effects of TPL on SH-SY5Y cell proliferation, apoptosis, and migration. Overexpression of miR-181a enhanced the TPL-induced activation of p38 mitogen-activated protein kinase (p38MAPK) and nuclear factor κ light chain enhancer of activated B cells (NF-κB) pathways. In conclusion, our research verified that TPL inhibited the proliferation and migration of human neuroblastoma SH-SY5Y cells by upregulating the expression of miR-181a.

摘要

神经母细胞瘤是 1 至 5 岁儿童癌症相关死亡的主要原因。迫切需要新的治疗策略和药物。本研究旨在探讨雷公藤红素（TPL）对神经母细胞瘤 SH-SY5Y 细胞增殖、迁移和凋亡的影响及其潜在的潜在机制。我们发现 TPL 抑制 SH-SY5Y 细胞活力、增殖和迁移，但诱导细胞凋亡。TPL 处理后 SH-SY5Y 细胞中基质金属蛋白酶-2（MMP-2）和 MMP-9 的表达减少。TPL 处理后 microRNA-181a（miR-181a）的表达上调。此外，抑制 miR-181a 逆转了 TPL 对 SH-SY5Y 细胞增殖、凋亡和迁移的影响。miR-181a 的过表达增强了 TPL 诱导的 p38 丝裂原活化蛋白激酶（p38MAPK）和核因子κ轻链增强子的激活 B 细胞（NF-κB）途径。总之，我们的研究证实，TPL 通过上调 miR-181a 的表达抑制人神经母细胞瘤 SH-SY5Y 细胞的增殖和迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c304/7844704/da9e56cc5e40/OR-26-1235-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c304/7844704/a762fe77e0d2/OR-26-1235-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c304/7844704/da9e56cc5e40/OR-26-1235-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c304/7844704/009bec91e8b9/OR-26-1235-g002.jpg
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