Cinnamaldehyde decreases the invasion and u-PA expression of osteosarcoma by down-regulating the FAK signalling pathway.
Shu-Chen ChuYih-Shou HsiehLi-Sung HsuChin-Yin LinYi-An LaiPei-Ni ChenPublished in: Food & function (2022)
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 in vitro and in vivo 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 N -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.
Keyphrases
- cell migration
- induced apoptosis
- endothelial cells
- signaling pathway
- poor prognosis
- single cell
- stem cells
- cell therapy
- cell cycle arrest
- type diabetes
- binding protein
- bone marrow
- pulmonary hypertension
- metabolic syndrome
- risk factors
- cardiovascular events
- escherichia coli
- cardiovascular disease
- coronary artery disease
- biofilm formation
- pluripotent stem cells
- mesenchymal stem cells
- induced pluripotent stem cells
- protein protein
- amino acid
- skeletal muscle
- protein kinase
- type iii
- candida albicans