Survivin inhibits anti-growth effect of p53 activated by aurora B |
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Authors: | Jung Ji-Eun Kim Tae-Kyung Lee Joong-Seob Oh Se-Yeong Kwak Sungwook Jin Xun Sohn Jin-Young Song Min-Keun Sohn Young-Woo Lee Soo-Yeon Pian Xumin Lee Jang-Bo Chung Yong Gu Choi Young Ki You Seungkwon Kim Hyunggee |
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Affiliation: | The Laboratory of Cell Growth and Function Regulation, College of Life and Environmental Sciences, Korea University, Seoul. |
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Abstract: | 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 beta-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. |
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Keywords: | Survivin, Aurora B p53 Glioblastoma Cell growth Cell death |
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