Department of Biochemistry, Dongguk University College of Oriental Medicine, Gyeongju 780-714, Korea.
Int J Oncol. 2010 Apr;36(4):867-72. doi: 10.3892/ijo_00000564.
High levels of mitotic progression-associated PLK1 and stress-associated HSF1 have been observed in various human cancers. In the present study, we investigated the effects of PLK1 and HSF1 knockdown on the proliferation of oral cancer cells using small interfering RNA. In human oral squamous cell carcinoma (SCC) tissues, the levels of PLK1 and HSF1 were higher compared to normal tissues. The expression levels of PLK1 and HSF1 were also elevated in the human oral SCC cell lines FaDu and HEp-2. Disruption of PLK1 induced cell cycle arrest at G2/M phase as well as apoptosis in oral cancer cells. Interestingly, knockdown of both PLK1 and HSF1 expression decreased cell proliferation while increasing apoptotic cell death in synergistic fashion. These results establish the potential value of PLK1 and HSF1 as targets for oral cancer therapy.
在各种人类癌症中观察到有丝分裂进展相关的 PLK1 和应激相关的 HSF1 水平升高。在本研究中，我们使用小干扰 RNA 研究了 PLK1 和 HSF1 敲低对口腔癌细胞增殖的影响。在人口腔鳞状细胞癌（SCC）组织中，PLK1 和 HSF1 的水平高于正常组织。PLK1 和 HSF1 的表达水平在人口腔 SCC 细胞系 FaDu 和 HEp-2 中也升高。PLK1 的破坏导致口腔癌细胞在 G2/M 期出现细胞周期停滞和凋亡。有趣的是，PLK1 和 HSF1 表达的同时敲低以协同方式降低细胞增殖，同时增加凋亡细胞死亡。这些结果确立了 PLK1 和 HSF1 作为口腔癌治疗靶点的潜在价值。
