去甲基斑蝥素通过抑制 FAK/Paxillin 和 F-肌动蛋白重排抑制 YD-15 细胞侵袭。
Norcantharidin Suppresses YD-15 Cell Invasion Through Inhibition of FAK/Paxillin and F-Actin Reorganization.
机构信息
Department of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 03080, Korea.
出版信息
Molecules. 2019 May 19;24(10):1928. doi: 10.3390/molecules24101928.
Norcantharidin (NCTD), a demethylated derivative of cantharidin, has been reported to exhibit activity against various types of cancers. However, the anti-invasive effects of NCTD and its molecular mechanism in human mucoepidermoid carcinoma (MEC) remain incompletely elucidated. Clonogenic, wound healing, invasion, zymography, western blotting and immunocytochemistry assays were performed in YD-15 cells to investigate the anti-invasive effect of NCTD and its molecular mechanism of action. The inhibitory effects of NCTD on invasiveness were compared with those of a novel focal adhesion kinase (FAK) kinase inhibitor, PF-562271. NCTD markedly suppressed the colony formation, migration, and invasion of YD-15 cells as well as the activities of MMP-2 and MMP-9. It disrupted F-actin reorganization through suppressing the FAK/Paxillin axis. Moreover, NCTD exhibited a powerful anti-invasive effect compared with that of PF-562271 in YD-15 cells. Collectively, these results suggest that NCTD has a potential anti-invasive activity against YD-15 cells. This study may clarify the impact of NCTD on migration and invasion of human MEC cells.
去甲基斑蝥素（NCTD）是斑蝥素的脱甲基衍生物，已被报道具有对抗多种类型癌症的活性。然而，NCTD 的抗侵袭作用及其在人黏液表皮样癌（MEC）中的分子机制仍不完全清楚。在 YD-15 细胞中进行集落形成、划痕愈合、侵袭、酶谱分析、western blot 和免疫细胞化学测定，以研究 NCTD 的抗侵袭作用及其作用机制。将 NCTD 的抑制侵袭作用与新型粘着斑激酶（FAK）激酶抑制剂 PF-562271 进行比较。NCTD 显著抑制 YD-15 细胞的集落形成、迁移和侵袭以及 MMP-2 和 MMP-9 的活性。它通过抑制 FAK/Paxillin 轴来破坏 F-肌动蛋白的重组。此外，NCTD 在 YD-15 细胞中表现出比 PF-562271 更强的抗侵袭作用。综上所述，这些结果表明 NCTD 对 YD-15 细胞具有潜在的抗侵袭活性。本研究可能阐明 NCTD 对人黏液表皮样癌细胞迁移和侵袭的影响。
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