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Scutellarin inhibits the metastasis and cisplatin resistance in glioma cells

Authors Tang S, Gao Y, Hu W

Received 13 September 2018

Accepted for publication 18 December 2018

Published 15 January 2019 Volume 2019:12 Pages 587—598


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 2

Editor who approved publication: Dr Federico Perche

Shi-lei Tang,1,* Yuan-lin Gao,2,* Wen-zhong Hu1

1Department of Neurosurgery, Huaihe Hospital of Henan University, Kaifeng 475000, Henan Province, China; 2Department of Neurology, Kaifeng Central Hospital, Kaifeng 475000, Henan Province, China

*These authors contributed equally to this work

Background: Scutellarin is a natural flavone compound that possesses anti-tumor and chemosensitization effects in several cancers. However, the effects of scutellarin on metastasis and chemoresistance in glioma have not been illustrated.
Methods: Glioma cells were treated with scutellarin in the presence or absence of LY294002. Cell proliferation was measured using a Cell Proliferation BrdU ELISA kit. Cell migration and invasion were analyzed using transwell assay. The expressions of E-cadherin, N-cadherin, vimentin, p-PI3K, PI3K, p-AKT, AKT, p-mTOR and mTOR were measured using Western blot. Furthermore, cells were incubated in the presence of cisplatin with or without the pretreatment of scutellarin. Cell viability was detected by the MTT assay. Cell apoptosis was measured using a histone/DNA ELISA detection kit. The expressions of ABCB1 and ABCG2 were detected using Western blot.
Results: In the present study, we found that scutellarin inhibited the proliferation, migration, and invasion of glioma cells. Scutellarin induced E-cadherin expression and reduced the expressions of N-cadherin, and vimentin in glioma cells. Our results also revealed that scutellarin enhanced chemosensitivity to cisplatin, as evidenced by the decreased cell viability to cisplatin and induced cell apoptosis. Moreover, scutellarin inhibited the expressions of ATP-binding cassette sub-family B member 1 and ATP-binding cassette sub-family G member 2 in cisplatin-resistant glioma cells. Scutellarin also prevented the activation of phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin pathway.
Conclusion: The data suggested that scutellarin suppressed metastasis and chemoresistance in glioma cells. Scutellarin might be a new therapeutic approach for the glioma therapy.

Keywords: glioma, scutellarin, metastasis, chemoresistance, PI3K/Akt/mTOR pathway

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