Regulation of Heat Shock-induced p53 Signaling in OC2 Human Oral Cancer Cells

中山醫學大學機構典藏 CSMUIR > 口腔醫學院 > 牙醫學系暨碩士班 > 期刊論文 > Item 310902500/10588

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/10588

Title:	Regulation of Heat Shock-induced p53 Signaling in OC2 Human Oral Cancer Cells
Authors:	Chou, Lin Shih-Shen Liao, Pao-Hsin Lee, Tien-Ling Yang, Shih-Huang Chou, Ming-Yung
Contributors:	中山醫學大學
Date:	2005
Issue Date:	2015-04-10T04:57:06Z (UTC)
Abstract:	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/ir/handle/310902500/10588
Relation:	中山醫學雜誌； 16 卷 2 期 (2005 / 12 / 01) ， P209 - 224
Appears in Collections:	[牙醫學系暨碩士班] 期刊論文

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