熱緊迫誘發人類口腔癌細胞p53訊息傅導之調節

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题名:	熱緊迫誘發人類口腔癌細胞p53訊息傅導之調節 Regulation of Heat Shock-induced p53 Signaling in OC2 Human Oral Cancer Cells
作者:	周林世珍;廖保鑫;李天翎;楊世煌;周明勇 Lin Shih-Shen Chou;Pao-Hsin Liao;Tien-Ling Lee;Shih-Huang Yang;Ming-Yung Chou
贡献者:	中山醫學大學
关键词:	過熱症;p53腫瘤抑制蛋白質;HSP70;PD98059;細胞凋亡 hyperthermia;HSP70;tumor suppressor protein p53;PD98059;apoptosis
日期:	2005-12-01
上传时间:	2010-08-06T04:01:00Z (UTC)
出版者:	教務處出版組
摘要:	背景：熱處理應用於腫瘤治療已數個世紀；然而，其作用機制仍莫衷一是。本實驗之目的乃在探討熱處理誘發人類口腔癌細胞之p53訊息傳導。材料與方法：人類口腔癌細胞株OC2或其未經熱處理細胞之蛋白質溶液經不同的熱處理（37、39、41及43℃，三小時）。利用免疫轉漬技術檢測調控細胞週期的主要調控分子之表現。以免疫沉澱法分析系統(NIH, Bethesda, MD, USA)分析。所有數據皆經ANOVA分析。結果：熱處理誘發p53積存、p53於serine 15位置磷酸化且增加其下游標的原因p21、Bax/Bcl-2之表。p53之表現於熱處理俊12小時達最高峰且至少延績達24小時。熱緊迫顯著增加p53與MDM2間之負回饋調控機制且增加ERKs的致活作用。PD98059, MEK （MAPK或ERK kinase）之特異抑制劑，顯著的強化了熱緊迫所誘發之p53磷酸化作用及HSP70的表現。HSP70係以單體存在且於熱處理後形成寡體。同時，HSP70複合物之表現例如p53、p21與Bax皆於熱處理後顯著增加。結論：本研究顯示熱處理誘發之細胞週期停滯及細胞凋亡係藉由p53之訊息傳導。此外，熱處理誘發之p53訊息傳導與HSP70表現與EPKs之活性無關。 Background: Heat treatment has been used in the treatment of tumors for centuries, though we know little about the heat-induced signaling pathway. This study investigates the regulation of heat shock-induced p53 signaling in OC2 cells, a human oral cancer cell line. Materials and methods: OC2 cells or cell lysates were incubated at different temperatures (37, 39, 41, and 43℃) for 3 hours. The Western blot was used to quantify differences in the master regulative molecule of cell cycle. Immunoprecipitation was used to detect the relationship among proteins, and non-denaturing electrophoresis to detect the conformation of HSP70. Patterns of change in expression were scanned and analyzed using the NIH image 1.56 software. All the data were analyzed by ANOVA. Results: Heat shock induced the accumulation of p53, phosphorylation of p53 at serine 15, and increased the expression of its downstream target genes, p21 and Bax/Bcl-2. The p53 signaling peaked at 12 hours and lasted for at least 24 hours after heat treatment. Heat shock significantly induced the negative control mechanism between p53 and MDM2 60 kDa fragment, triggered the activation of ERKs. PD98059, a specific inhibitor of MEK (MAPK or ERK kinase), and markedly enhanced the heat shock-induced p53 phosphorylation and HSP70 expression. After heat shock, HSP70 was found to exist monomeric form and to be oligomerized. At the same time, heat shock significantly induced the expression of such HSP70 complexes as p53, p21 and Bax. Conclusion: Heat-induced cell cycle arrest and apoptosis are mediated by the activation of p53 signaling. The p53 signaling and HSP70 expression induced by heat shock occur independent of ERKs activation.
URI:	https://ir.csmu.edu.tw:8080/handle/310902500/2010
關聯:	中山醫學雜誌, v16 n.2 p209-224
显示于类别:	[教務處] 期刊論文

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