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Cryptotanshinone inhibits esophageal squamous-cell carcinoma in vitro and in vivo through the suppression of STAT3 activation

Authors Ji Y, Liu Y, Xue N, Du T, Wang L, Huang R, Li L, Yan C, Chen X

Received 16 September 2018

Accepted for publication 3 January 2019

Published 29 January 2019 Volume 2019:12 Pages 883—896


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 2

Editor who approved publication: Professor Jianmin Xu

Yubin Ji,1 Yichen Liu,1,2 Nina Xue,2 Tingting Du,2 Liyuan Wang,2 Rui Huang,2 Ling Li,2 Chunhong Yan,3 Xiaoguang Chen2

1Research Center on Life Sciences and Environmental Sciences, Harbin University of Commerce, Harbin 150076, People’s Republic of China; 2State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, People’s Republic of China; 3Georgia Cancer Center, Augusta University, Augusta, GA, USA

Purpose: Esophageal squamous-cell carcinoma (ESCC) is the most common subtype of esophageal cancer, with a poor clinical outcome. Cryptotanshinone (CTS) is the main bioactive compound from the root of Salvia miltiorrhiza Bunge. Our study aimed to investigate the anti-cancer effects and molecular mechanisms of CTS on ESCC.
Materials and methods: We investigated the anti-tumor activity of CTS on ESCC in vitro and in vivo. Activation of the STAT3 signaling pathway was evaluated in ESCC and HEK-Blue™ IL-6 cells. Cell viability was assessed by the MTT assay. Apoptosis and cell cycle arrest were assessed using flow cytometry. Cell migration was detected by a scratch wound assay.
Results: CTS inhibited STAT3 expression and IL-6-mediated STAT3 activation in esophageal cancer cells. Subsequently, CTS dose-dependently inhibited the proliferation of esophageal cancer cells via induction of cell apoptosis. Furthermore, CTS suppressed the migration of esophageal cancer cells. In vivo, CTS inhibited tumor growth of EC109 cell in xenograft mice without any obvious effect on body weight.
Conclusion: Our results indicated that STAT3 inhibition may be a therapeutic target for esophageal cancer. CTS could provide a potential approach for esophageal cancer therapy by influencing the janus kinase-2/STAT3 signaling pathway.

Keywords: xenograft, CTS, ESCC, proliferation, apoptosis, migration

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