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Luteolin suppresses tumor proliferation through inducing apoptosis and autophagy via MAPK activation in glioma

Authors You Y, Wang R, Shao N, Zhi F, Yang Y

Received 17 October 2018

Accepted for publication 4 February 2019

Published 28 March 2019 Volume 2019:12 Pages 2383—2396


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 3

Editor who approved publication: Dr William Cho

Yijie You,1–3 Rong Wang,2 Naiyuan Shao,1–3 Feng Zhi,1,2 Yilin Yang1–3

1Department of Neurosurgery, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China; 2Modern Medical Research Center, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China; 3Department of Neurosurgery, The First People’s Hospital of Changzhou, Changzhou, Jiangsu, China

Purpose: Glioma is a malignant tumor that originates in the brain and spine and is difficult to be completely removed. Though glioma patients receive active treatment, the survival rate is still poor. Therefore, it is urgent to discover a new medicine to treat glioma patients in order to improve the survival rate. In this study, we explored the anticancer effect and the potential mechanism of luteolin on glioma in vitro.
Materials and methods: Cell viability was determined by Cell Counting Kit-8 (CCK-8) assay. Fluorescent microscopy and flow cytometry analysis were used to determine the cellular apoptosis. Western blot analysis was performed to explore the changes in protein expression. Quantitative reverse transcription-PCR (qRT-PCR) analysis was utilized to evaluate the expression level of the tumor suppressor miR-124-3p.
Results: CCK-8 assays indicated that luteolin significantly inhibited glioma cell proliferation in a time- and dose-dependent manner. Fluorescent microscopy and flow cytometry analysis confirmed that luteolin induced glioma cell apoptosis. Western blot analysis showed that luteolin induced cellular apoptosis in glioma cells via MAPK activation (JNK, ERK, and p38). Luteolin stimulated the death receptor (FADD) to regulate the apoptosis proteins (Caspase-8, Caspase-3, and PARP). Luteolin increased the expression levels of LC3B II/I and downregulated the level of p62 that promotes cell autophagy. Finally, qRT-PCR confirmed that luteolin upregulated the expression levels of miR-124-3p.
Conclusion: These findings illustrate that luteolin may be a potential drug for glioma treatment.

Keywords: glioma, luteolin, apoptosis, autophagy, miR-124-3p

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