n/a
Abstract Title:

Eriodictyol inhibits glioblastoma migration and invasion by reversing EMT via downregulation of the P38 MAPK/GSK-3β/ZEB1 pathway.

Abstract Source:

Eur J Pharmacol. 2021 Jun 5 ;900:174069. Epub 2021 Mar 31. PMID: 33811837

Abstract Author(s):

Feng Lv, Qian Du, Lin Li, Xin Xi, Qinglong Liu, Wenjun Li, Songqing Liu

Article Affiliation:

Feng Lv

Abstract:

Eriodictyol (ERD) is a natural flavonoid that exists in many vegetables and fruits, especially citrus fruits. It has been proven to have many pharmacological effects, such as antioxidative, anti-inflammatory and neuroprotective effects. Our previous study showed that eriodictyol could inhibit the proliferation and induce the apoptosis of glioblastoma cells by downregulating the PI3K/Akt/NF-κB pathway and restraining its migration and invasion. However, the mechanism by which eriodictyol prevents glioblastoma metastasis is still unknown. Epithelial-mesenchymal transition (EMT) is a key process for many cancer metastases; it also confers locomotivity to tumor cells, including glioblastoma. In this study, we found that eriodictyol can suppress the migration and invasion of glioblastoma A172 and U87 MG cell lines by suppressing the EMT markers - N-cadherin and E-cadherin through Wound healing and Transwell assays, Western blot, RT-qPCR, immunofluorescence and immunohistochemistry.Further research revealed that the mechanism could be connected with downregulation of the P38 MAPK/GSK-3β/ZEB1 signaling pathway. These findings can provide a new idea for the treatment of glioblastoma.

Study Type : In Vitro Study

Print Options


Key Research Topics

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2024 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.