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      Cinnamaldehyde Inhibits the Function of Osteosarcoma by Suppressing the Wnt/β-Catenin and PI3K/Akt Signaling Pathways

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          Abstract

          Background

          Osteosarcoma (OS) is a primary bone tumor associated with locally aggressive growth and early metastatic potential that typically occurs in children and adolescents. Chinese traditional medicine Cinnamomum cassia Presl has been shown to have significant tumor-killing effect, in which cinnamaldehyde (CA) is the main active ingredient.

          Purpose

          To explore the anticancer effect of CA on the osteosarcoma cells and the possible molecular mechanism.

          Methods

          Crystal violet assay, MTT assay and colony-forming assay were used to confirm the inhibitory role of CA in the proliferation of 143B and MG63 osteosarcoma cells. Hoechst 33258 staining and flow cytometry were used to observe apoptosis. The migration and invasion role of OS cells were evaluated using transwell assays and wound healing assays. Western blotting was used to analyse the protein expression levels. Nude mice were inoculated with 143B cells to establish an orthotopic OS tumor animal model and to investigate the effects of CA on OS tumors.

          Results

          According to crystal violet assay, MTT assay and colony-forming assay, CA significantly inhibited cell proliferation. Hoechst 33258 staining and flow cytometry analysis showed that CA-induced apoptosis in a concentration-dependent manner. In addition, transwell assays and wound healing assays showed that CA inhibited the migration and invasion of osteosarcoma cells. In vivo mouse models, CA inhibited the growth of osteosarcoma. The potential mechanisms could be that CA inhibited the transcriptional activity of Wnt/β-catenin and PI3K/Akt of the osteosarcoma.

          Conclusion

          CA may inhibit the proliferation, migration, invasion and promote apoptosis of OS cells by inhibiting Wnt/β-catenin and PI3K/Akt signaling pathways. CA may be a potentially effective anti-tumor drug.

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          Most cited references 40

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          Epithelial-mesenchymal transitions in development and disease.

          The epithelial to mesenchymal transition (EMT) plays crucial roles in the formation of the body plan and in the differentiation of multiple tissues and organs. EMT also contributes to tissue repair, but it can adversely cause organ fibrosis and promote carcinoma progression through a variety of mechanisms. EMT endows cells with migratory and invasive properties, induces stem cell properties, prevents apoptosis and senescence, and contributes to immunosuppression. Thus, the mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.
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            Matrix metalloproteinases: regulators of the tumor microenvironment.

            Extracellular proteolysis mediates tissue homeostasis. In cancer, altered proteolysis leads to unregulated tumor growth, tissue remodeling, inflammation, tissue invasion, and metastasis. The matrix metalloproteinases (MMPs) represent the most prominent family of proteinases associated with tumorigenesis. Recent technological developments have markedly advanced our understanding of MMPs as modulators of the tumor microenvironment. In addition to their role in extracellular matrix turnover and cancer cell migration, MMPs regulate signaling pathways that control cell growth, inflammation, or angiogenesis and may even work in a nonproteolytic manner. These aspects of MMP function are reorienting our approaches to cancer therapy. Copyright 2010 Elsevier Inc. All rights reserved.
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              Activation of epithelial-mesenchymal transition (EMT) is important for cancer cell dissemination. Two papers in this issue of Cancer Cell (Ocaña and colleagues and Tsai and colleagues) support the concept that the reversal of EMT is necessary for efficient metastatic colonization. Moreover, although EMT has been associated with stemness properties, one study indicates that they are not necessarily linked. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                dddt
                dddt
                Drug Design, Development and Therapy
                Dove
                1177-8881
                30 October 2020
                2020
                : 14
                : 4625-4637
                Affiliations
                [1 ]Department of Orthopedics, The First Affiliated Hospital of Chongqing Medical University , Chongqing 400016, People’s Republic of China
                [2 ]Department of Dermatology, The First Affiliated Hospital of Chongqing Medical University , Chongqing 400016, People’s Republic of China
                [3 ]Key Laboratory of Clinical Diagnosis of Education Ministry, College of Laboratory Medicine, Chongqing Medical University , Chongqing 400016, People’s Republic of China
                Author notes
                Correspondence: Xiaoji Luo Department of Orthopedics, The First Affiliated Hospital of Chongqing Medical University , Chongqing400016, People’s Republic of ChinaTel +86-18523123100Fax +86 2389012820 Email cy2982@163.com
                Jinyong Luo College of Laboratory Medicine, Chongqing Medical University , Chongqing400016, People’s Republic of ChinaTel +86-13637738426Fax +86 2368485239 Email luojinyong888@hotmail.com
                Article
                277160
                10.2147/DDDT.S277160
                7608596
                © 2020 Huang et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 6, References: 40, Pages: 13
                Funding
                Funded by: National Natural Science Foundation of China, open-funder-registry 10.13039/501100001809;
                This study was supported by the National Natural Science Foundation of China (NO.81873998).
                Categories
                Original Research

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