Impact Factor 4.137 | CiteScore 4.28
More on impact ›

Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Oncol. | doi: 10.3389/fonc.2019.00752

Magnolol Suppresses TGF-β–Induced Epithelial-to-Mesenchymal Transition in Human Colorectal Cancer Cells

Sungwoo Chei1, Hyun-Ji Oh1, Ji-Hyeon Song1, Young-Jin Seo1, Kippeum Lee1, Heegu Jin1, Jae-Hoon Oh1 and  Boo-Yong Lee1*
  • 1CHA University, South Korea

Tumor metastasis is the end state of a multistep process that includes dissemination of tumor cells to distant organs and requires tumor cells to adapt to different tissue microenvironments. During metastasis, tumor cells undergo a morphological change known as transdifferentiation or the epithelial-to-mesenchymal transition (EMT). In normal embryonic development, the EMT occurs in the context of morphogenesis in a variety of tissues. Over the course of this process, epithelial cells lose their cell–cell adhesion and polarity properties. In this study, we investigated whether magnolol could suppress the EMT in human colorectal cancer cells. To this end, we examined the epithelial markers E-cadherin, ZO-1, and claudin and the mesenchymal markers N-cadherin, TWIST1, Slug, and Snail. Magnolol effectively inhibited EMT in human colon cancer cell lines by upregulating epithelial markers and downregulating mesenchymal markers. The EMT is induced by the TGF-β signaling pathway. To determine whether magnolol disrupts TGF-β signaling, we examined several mediators of this pathway, and found that magnolol decreased the levels of phosphorylated (i.e., active) ERK, GSK3β, and Smad. We conclude that magnolol blocks migration in HCT116 cells by suppressing TGF-β signaling.

Keywords: Tumor metastasis, colorectal cancer, Magnolol (PubChem CID: 72300), Epithelial to mesenchymal (EMT), TGF - β1

Received: 09 May 2019; Accepted: 26 Jul 2019.

Copyright: © 2019 Chei, Oh, Song, Seo, Lee, Jin, Oh and Lee. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Boo-Yong Lee, CHA University, Seongnam, Gyeonggi, South Korea, bylee@cha.ac.kr