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Baohuoside I via mTOR Apoptotic Signaling to Inhibit Glioma Cell Growth

Authors Guo Y, Wang C, Jiang M, Zhu H, Weng M, Sun L, Zhang Y

Received 17 June 2020

Accepted for publication 24 September 2020

Published 10 November 2020 Volume 2020:12 Pages 11435—11444


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Kenan Onel

Yangyang Guo,1,* Cheng Wang,1,* Minghui Jiang,1 Hengyue Zhu,1 Min Weng,1 Linxiao Sun,1 Yanlei Zhang2

1Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, Zhejiang Provincial Top Key Discipline in Surgery, Wenzhou Medical University First Affiliated Hospital, Wenzhou, Zhejiang, People’s Republic of China; 2Neurology Department, Wenzhou Medical University First Affiliated Hospital, Wenzhou, Zhejiang, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Yanlei Zhang; Linxiao Sun Email [email protected]; [email protected]

Introduction: Baohuoside I, a novel oncotherapeutic agent, has been reported to have anti-cancer effects on a variety of cancers, but its role in glioma and its molecular mechanism are still unclear.
Methods: The proliferation of U251 cells was detected by real-time cellular analysis (RTCA), CCK-8, Ki67 immunofluorescence and colony formation assay. The effect of Baohuoside I on the invasion and migration of U251 cells was measured by transwell and scratch tests. The apoptosis of U251 cells was detected by flow cytometry. The expression level of related protein was detected by western blotting.
Results: Baohuoside I could inhibit the proliferation of human glioma cells and induce apoptosis. Further study showed that the migration and invasion ability of glioma was significantly decreased by Baohuoside I. Western blot revealed the expression of p-AMPKα 1 protein was up-regulated, and the expression of p-mTOR and p-S6K was down-regulated after Baohuoside I treatment. Tumorigenesis in nude mice showed that Baohuoside I had an anti-glioma effect in vivo.
Conclusion: We propose a natural product, which can inhibit the proliferation, invasion and migration of glioma and may be a valuable anti-tumor candidate. The inhibitory effect of Baohuoside I on the glioma is achieved by inducing the apoptosis of the tumor cells, rather than autophagy. In addition, the pathway to induce cell apoptosis of Baohuoside I is to target the mTOR signal.

Keywords: Baohuoside I, mTOR, glioma, apoptosis, proliferation

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