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Research Paper|Volume 12, Issue 10|pp 9714—9725

Qigesan inhibits esophageal cancer cell invasion and migration by inhibiting Gas6/Axl-induced epithelial-mesenchymal transition

Lingyu Kong1, Xin Lu2, Xuanyu Chen1, Yunyan Wu3, Yushuang Zhang4, Huijuan Shi4, Jing Li1,4
  • 1College of Integrated Chinese and Western Medicine, Hebei Medical University, Shijiazhuang 050017, Hebei, China
  • 2Department of Clinical Laboratory, Tangshan Maternal and Children Hospital, Tangshan 063000, Hebei, China
  • 3Research Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, Hebei, China
  • 4Department of Traditional Chinese Medicine, Tumor Hospital of Hebei Province, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, Hebei, China
* Equal contribution
Received: January 14, 2020Accepted: March 31, 2020Published: May 20, 2020
https://doi.org/10.18632/aging.103238

Copyright © 2020 Kong et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Qigesan (QGS) has been used to effectively treat esophageal cancer (EC) for decades in China, but the mechanism by which it suppresses EC metastasis remains unknown. In this study, we examined the effects of QGS on EC cell mobility. Using immunohistochemistry and immunofluorescence, expression of Gas6 and Axl, which promote tumor cell migration and invasion, was examined in carcinoma tissues and adjacent normal tissues from EC patients. Levels of Gas6, Axl, and the Gas6/Axl complex were also examined in ECA109 and TE13 EC cells treated with QGS. In addition, immunofluorescent staining and quantitative protein analysis were used to examine E-cadherin, N-cadherin, and Snail levels in ECA109 and TE13 EC cells after QSG administration, and cell mobility was assessed. The results demonstrated that levels of Gas6 and Axl expression are higher in EC tissues than in adjacent normal tissues. Moreover, QGS decreased Gas6/Axl levels, increased E-cadherin expression, decreased Snail and N-cadherin expression, and inhibited epithelial-mesenchymal transition (EMT) in EC cells. QGS thus suppresses EMT in EC by inhibiting Gas6/Axl binding.