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

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, Xumin Pian, Jang Bo Lee, Yong Gu Chung, Ki Choi Young, Seungkwon You, Hyunggee Kim

Research output: Contribution to journalArticle

16 Citations (Scopus)

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 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.

Original languageEnglish
Pages (from-to)1164-1171
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume336
Issue number4
DOIs
Publication statusPublished - 2005 Nov 4

Fingerprint

Tumors
Apoptosis
Glioblastoma
Growth
Aurora Kinase B
Galactosidases
Astrocytes
Cell Proliferation
Cell proliferation
Cell growth
Neoplasms
Centrosome
Amplification
Genomic Instability
Genes
Tumor Cell Line
Chemical activation
Cells
Carcinogenesis
Pharmaceutical Preparations

Keywords

  • Aurora B
  • Cell death
  • Cell growth
  • Glioblastoma
  • p53
  • Survivin

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Survivin inhibits anti-growth effect of p53 activated by aurora B. / 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; Young, Ki Choi; You, Seungkwon; Kim, Hyunggee.

In: Biochemical and Biophysical Research Communications, Vol. 336, No. 4, 04.11.2005, p. 1164-1171.

Research output: Contribution to journalArticle

Jung, JE, Kim, TK, Lee, JS, Oh, SY, Kwak, S, Jin, X, Sohn, JY, Song, MK, Sohn, YW, Lee, SY, Pian, X, Lee, JB, Chung, YG, Young, KC, You, S & Kim, H 2005, 'Survivin inhibits anti-growth effect of p53 activated by aurora B', Biochemical and Biophysical Research Communications, vol. 336, no. 4, pp. 1164-1171. https://doi.org/10.1016/j.bbrc.2005.08.235
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 ; Young, Ki Choi ; You, Seungkwon ; Kim, Hyunggee. / Survivin inhibits anti-growth effect of p53 activated by aurora B. In: Biochemical and Biophysical Research Communications. 2005 ; Vol. 336, No. 4. pp. 1164-1171.
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