Survivin inhibits anti-growth effect of p53 activated by aurora B

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• 作者：Ji-Eun Jung ; Tae-Kyung Kim ; Joong-Seob Lee ; Se-Yeong Oh ; Sungwook Kwak ; Xun Jin ; Jin-Young Sohn ; Min-Keun Song ; Young-Woo Sohn ; Soo-Yeon Lee et al.
• 关键词：Survivin ; Aurora B ; p53 ; Glioblastoma ; Cell growth ; Cell death
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2005
• 出版时间：2005
• 年：2005
• 卷：336
• 期：4
• 页码：1164-1171
• 全文大小：465 K

文摘

Genomic instability and apoptosis evasion are hallmarks of cancer, but the molecular mechanisms governing these processes remain elusive. Here, we found that survivin, a member of the apoptosis-inhibiting gene family, and aurora B kinase, a chromosomal passenger protein, were co-overexpressed in the various glioblastoma cell lines and tumors. Notably, exogenous introduction of the aurora B in human BJ cells was shown to decrease cell growth and increase the senescence-associated β-galactosidase activity by activation of p53 tumor suppressor. However, aurora B overexpression failed to inhibit cell proliferation in BJ and U87MG cells transduced with dominant-negative p53 as well as in p53^−/− mouse astrocytes. Aurora B was shown to increase centrosome amplification in the p53^−/− astrocytes. Survivin was shown to induce anchorage-independent growth and inhibit anti-proliferation and drug-sensitive apoptosis caused by aurora B. Overexpression of both survivin and aurora B further accelerated the proliferation of BJ cells. Taken together, the present study indicates that survivin should accelerate tumorigenesis by inhibiting the anti-proliferative effect of p53 tumor suppressor that is activated by aurora B in normal and glioblastoma cells containing intact p53.