The antitumor effect of PLK1 and HSF1 double knockdown on human oral carcinoma cells
The antitumor effect of PLK1 and HSF1 double knockdown on human oral carcinoma cells
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DOI：
10.3892/ijo_00000564
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发表时间：
2010-04-01
影响因子：
5.2
通讯作者：
Ahn, Sang-Gun
中科院分区：
文献类型：
--
作者：
Kim, Soo-A;Kwon, Seong-Min;Ahn, Sang-Gun
在各种人类癌症中观察到高水平的有丝分裂进展相关PLK1和应激相关HSF1。在本研究中，我们研究了PLK1和HSF1敲低对口腔癌细胞增殖的影响，使用小干扰RNA。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的表达水平也在人口腔鳞癌细胞系FaDu和HEp-2中升高。PLK1的破坏诱导口腔癌细胞的细胞周期停滞在G2/M期以及凋亡。有趣的是，PLK1和HSF1表达的敲低降低了细胞增殖，同时以协同方式增加了凋亡性细胞死亡。这些结果确立了PLK1和HSF1作为口腔癌治疗靶点的潜在价值。
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.