Open Access
ARTICLE
Triptolide Inhibits Proliferation and Migration of Human Neuroblastoma SH-SY5Y Cells by Upregulating MicroRNA-181a
* 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
‡ Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, P.R. China
Oncology Research 2018, 26(8), 1235-1243. https://doi.org/10.3727/096504018X15179661552702
31 July 2024 Editors Note:
Readers are alerted that concerns were raised about the integrity of some of the data presented in the article. Further editorial action will be taken once this matter has been resolved.
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 k light chain enhancer of activated B cells (NF-kB) 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.Keywords
Cite This Article
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.