School of Dentistry, Chung Shan Medical University, Taichung 40201, Taiwan ; Department of Dentistry, Chung Shan Medical University Hospital, Taichung 40201, Taiwan.
Evid Based Complement Alternat Med. 2012;2012:732578. doi: 10.1155/2012/732578. Epub 2012 Dec 18.
Caffeic acid phenethyl ester (CAPE), an active component extracted from honeybee hives, exhibits anti-inflammatory and anticancer activities. However, the molecular mechanism by which CAPE affects oral cancer cell metastasis has yet to be elucidated. In this study, we investigated the potential mechanisms underlying the effects of CAPE on the invasive ability of SCC-9 oral cancer cells. Results showed that CAPE attenuated SCC-9 cell migration and invasion at noncytotoxic concentrations (0 μM to 40 μM). Western blot and gelatin zymography analysis findings further indicated that CAPE downregulated matrix metalloproteinase-2 (MMP-2) protein expression and inhibited its enzymatic activity. CAPE exerted its inhibitory effects on MMP-2 expression and activity by upregulating tissue inhibitor of metalloproteinase-2 (TIMP-2) and potently decreased migration by reducing focal adhesion kinase (FAK) phosphorylation and the activation of its downstream signaling molecules p38/MAPK and JNK. These data indicate that CAPE could potentially be used as a chemoagent to prevent oral cancer metastasis.
咖啡酸苯乙酯（CAPE）是从蜂箱中提取的一种具有抗炎和抗癌活性的有效成分。然而，CAPE 影响口腔癌细胞转移的分子机制尚不清楚。在这项研究中，我们研究了 CAPE 对 SCC-9 口腔癌细胞侵袭能力的潜在作用机制。结果表明，CAPE 在非细胞毒性浓度（0μM 至 40μM）下可减弱 SCC-9 细胞的迁移和侵袭。Western blot 和明胶酶谱分析结果进一步表明，CAPE 下调基质金属蛋白酶-2（MMP-2）蛋白表达并抑制其酶活性。CAPE 通过上调组织金属蛋白酶抑制剂-2（TIMP-2）来发挥对 MMP-2 表达和活性的抑制作用，并通过降低粘着斑激酶（FAK）磷酸化和其下游信号分子 p38/MAPK 和 JNK 的激活来强力减少迁移。这些数据表明，CAPE 可能可用作预防口腔癌转移的化疗药物。
