<i>Cinnamomum bejolghota</i> Extract Inhibits Colorectal Cancer Cell Metastasis and TGF-β1-Induced Epithelial-Mesenchymal Transition via Smad and Non-Smad Signaling Pathway

<i>Cinnamomum bejolghota</i>, used in Thai traditional medicine remedies, has several biological activities including antimicrobial, antifungal, and anticancer. In colorectal cancer, epithelial-mesenchymal transition (EMT) is an initial step of cancer metastasis. Thus, this study investi...

Full description

Saved in:
Bibliographic Details
Main Authors: Athicha Kittiwattanokhun (Author), Sukanda Innajak (Author), Etsu Tashiro (Author), Masaya Imoto (Author), Ramida Watanapokasin (Author)
Format: Book
Published: MDPI AG, 2022-05-01T00:00:00Z.
Subjects:
Online Access:Connect to this object online.
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:<i>Cinnamomum bejolghota</i>, used in Thai traditional medicine remedies, has several biological activities including antimicrobial, antifungal, and anticancer. In colorectal cancer, epithelial-mesenchymal transition (EMT) is an initial step of cancer metastasis. Thus, this study investigated the effects of <i>C. bejolghota</i> bark extract (CBE) on colorectal cancer cell metastasis and transforming growth factor-β1 (TGF-β1) induced EMT in LoVo cells. The results showed that CBE could reduce cell migration, invasion, and adhesion of LoVo cells in a dose-dependent manner. In addition, our studies also showed that CBE could reverse TGF-β1-induced morphological changes as well as increase an epithelial marker, E-cadherin, while the expression of the mesenchymal marker, N-cadherin, was decreased in TGF-β1-treated LoVo cells. MMP-2 expression was effectively decreased but TIMP-1 and TIMP-2 expression was increased by the CBE treatment in LoVo cells. CBE also inhibited Smad2/3 phosphorylation and nuclear translocation as well as decreased the expression of Snail, Slug, and TCF8/ZEB1 transcription factors in LoVo cells. Moreover, CBE could inhibit TGF-β1-induced Smad-independent signaling pathway by decreased phosphorylation of ERK1/2, p38, and Akt. These findings suggest that CBE inhibited TGF-β1-induced EMT in LoVo cells via both Smad-dependent and Smad-independent pathways. Therefore, CBE may function as an alternative therapeutic treatment for colorectal cancer metastasis.
Item Description:10.3390/scipharm90020030
2218-0532
0036-8709