Silencing heat shock transcription factor 1 using small interfering RNA enhances mild hyperthermia and hyperthermia sensitivity in human oral squamous cell carcinoma cells

Y. Tabuchi, Yukihiro Furusawa, S. Wada, K. Ohtsuka, T. Kondo
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引用次数: 9

Abstract

Hyperthermia(HT)for various types of malignant tumor is a promising agent in anti-tumor action. However,the acquisition of thermotolerance in carcinoma cells due to the induction of heat shock proteins(HSPs)makes HT less effective. Recent findings suggest that a decrease in heat shock transcription factor 1 (HSF1) elicits sensitivity to HT in some kinds of carcinoma cells. Here we evaluated the effects of knockdown of HSF1 by small interfering RNA(siRNA)on the sensitivity to mild hyperthermia (MHT) and HT in human oral squamous cell carcinoma (OSCC) cells. Treatment of human OSCC HSC-3 cells with siHSF1-2,a siRNA for HSF1,effectively decreased the protein expression level of HSF1 in a time-dependent manner at 37°C, and almost complete knockdown of HSF1 was observed at 48 h post treatment. Moreover,although a remarkable elevation of protein expression of HSPs such as Hsp70,Hsp40 and Hsp27 was detected in HSC-3 cells treated with MHT at 42°C and HT at 44°C for 90 min,expression of these HSPs was significantly decreased in HSF1-silenced cells under normal and hyperthermic conditions. In HSC-3 cells,knockdown of HSF1 significantly decreased the number of viable cells at 37°C, suggesting that HSF1 may be required for normal cell growth. In addition,sensitivity to MHT or HT was markedly enhanced in HSF1-silenced HSC-3 cells. Moreover, we observed an increase in sensitivity to these hyperthermic treatments by silencing of HSF1 in human OSCC cell lines HO-1-N-1,HO-1-u-1 and SAS. These findings indicate that silencing of HSF1 enhances sensitivity to MHT and HT in human OSCC cells,and that hyperthermic treatment combined with HSF1 silencing has potential significance in OSCC therapy. HSF1 siRNA enhances thermosensitivity・Y.Tabuchi et al. ― ― 99 Received 22 November,2011,Accepted 1 December,2011. Corresponding author;Tel,+81-76-434-7185;Fax,+81-76-434-5176; e-mail,ytabu@cts.u-toyama.ac.jp doi:10.3191/thermalmed.27.99 ©2011 Japanese Society for Thermal Medicine
使用小干扰RNA沉默热休克转录因子1增强人口腔鳞状细胞癌细胞的轻度热疗和热疗敏感性
热疗治疗各种类型的恶性肿瘤是一种很有前途的抗肿瘤药物。然而,由于热休克蛋白(HSPs)的诱导,癌细胞获得了耐热性,使得高温疗法的效果降低。最近的研究结果表明,热休克转录因子1 (HSF1)的降低引起某些类型的癌细胞对热休克的敏感性。本研究评估了小干扰RNA(siRNA)敲低HSF1对人口腔鳞状细胞癌(OSCC)细胞对轻度高温(MHT)和高温敏感性的影响。用HSF1的siRNA sihsf1 - 1-2处理人OSCC HSC-3细胞,在37℃时,HSF1蛋白的表达水平呈时间依赖性降低,在处理后48 h, HSF1几乎完全被敲除。此外,尽管在42°C MHT和44°C HT处理90 min的hsf1 -3细胞中检测到Hsp70、Hsp40和Hsp27等热休克蛋白的表达显著升高,但在正常和高温条件下,hsf1沉默细胞中这些热休克蛋白的表达显著降低。在HSC-3细胞中,37°C时敲低HSF1显著降低活细胞数量,提示正常细胞生长可能需要HSF1。此外,hsf1沉默的HSC-3细胞对MHT或HT的敏感性显著增强。此外,我们通过沉默人OSCC细胞系HO-1-N-1、HO-1-u-1和SAS中的HSF1,观察到对这些高温处理的敏感性增加。这些发现表明,HSF1沉默可增强人OSCC细胞对MHT和HT的敏感性,热疗联合HSF1沉默在OSCC治疗中具有潜在意义。HSF1 siRNA增强热敏性。Tabuchi et al. 2011年11月22日收稿,2011年12月1日收稿。通讯作者,电话+ 81-76-434-7185,传真+ 81-76-434-5176;e-mail,ytabu@cts.u-toyama.ac.jp doi:10.3191/thermalmed.27.99©2011日本热医学学会
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