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肉桂醛通过下调 FAK 信号通路降低骨肉瘤的侵袭和 u-PA 的表达。

Cinnamaldehyde decreases the invasion and u-PA expression of osteosarcoma by down-regulating the FAK signalling pathway.

机构信息

Institute and Department of Food Science, Central Taiwan University of Science and Technology, Taichung, Taiwan.

Department of Biochemistry, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.

出版信息

Food Funct. 2022 Jun 20;13(12):6574-6582. doi: 10.1039/d2fo00634k.

DOI:10.1039/d2fo00634k
PMID:35678522
Abstract

Cancer metastasis is the major cause of the high mortality risk of patients with osteosarcoma. Cinnamaldehyde has been shown to exhibit multiple tumour-suppressing activities, but its role in human osteosarcoma is not yet completely defined. In this study, the antimetastatic effect of cinnamaldehyde on highly metastatic human osteosarcoma cells was observed and using Saos-2 and 143B cells. Cinnamaldehyde reduced the activity and protein level of urokinase-type plasminogen activator (u-PA) and suppressed the invasion ability of osteosarcoma cells by inhibiting the phosphorylation of focal adhesion kinase. In addition, cinnamaldehyde reduced cell movement, cell-matrix adhesion, and the expression of the mesenchymal markers of epithelial-to-mesenchymal transition, namely, fibronectin and -cadherin. Importantly, the oral administration of cinnamaldehyde remarkably suppressed the pulmonary metastasis of osteosarcoma in mice. Results indicated that cinnamaldehyde has therapeutic potential for inhibiting osteosarcoma metastasis.

摘要

癌症转移是骨肉瘤患者高死亡率的主要原因。肉桂醛具有多种肿瘤抑制作用,但它在人类骨肉瘤中的作用尚未完全确定。在这项研究中,观察到肉桂醛对高转移性人骨肉瘤细胞 Saos-2 和 143B 细胞的抗转移作用。肉桂醛通过抑制粘着斑激酶的磷酸化来降低尿激酶型纤溶酶原激活物(u-PA)的活性和蛋白水平,并抑制骨肉瘤细胞的侵袭能力。此外,肉桂醛降低了细胞运动、细胞-基质黏附以及上皮-间充质转化的间充质标志物纤连蛋白和 E-钙黏蛋白的表达。重要的是,肉桂醛的口服给药显著抑制了骨肉瘤在小鼠中的肺转移。结果表明,肉桂醛具有抑制骨肉瘤转移的治疗潜力。

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