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

Jung, Jieun; Kim, Tae‐Kyung; Lee, Joong-Seob; Oh, Sang-Ho; Kwak, Sungwook; Jin, Xun; Sohn, Jinyoung; Song, Min-Keun; Sohn, Young-Woo; Lee, Sooyeon; Pian, Xumin; Lee, Jang-Bo; Chung, Yong Gu; Choi, Young Ki; You, Seungkwon; Kim, Hyunggee

doi:10.1016/j.bbrc.2005.08.235

Cited by 19 publications

(12 citation statements)

References 29 publications

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“…Aurora-B kinase exists in a complex with survivin and INCENP and its kinase activity is stimulated by survivin binding and phosphorylation [5]. Survivin may promote tumorigenesis and progression by suppressing the antiproliferate effect of p53 tumor suppressor activated by Aurora-B overexpression in normal cells and glioblastoma cells containing intact p53 gene [11]. A recent finding shows that the activity of survivin, Aurora-B, and INCENP are responsible for oncogenic Ras-mediated cell transformation and lead to an accelerated growth of tumor cells [13,26].…”

Section: Discussionmentioning

confidence: 99%

Aurora-B expression and its correlation with cell proliferation and metastasis in oral cancer

et al. 2007

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Aurora-B kinase is a chromosomal passenger protein and is essential for chromosome segregation and cytokinesis. Aurora-B overexpression in various cancer cells induces chromosomal number instability to produce multinuclearity and relates to metastasis. Here, we examined the expression of Aurora-B in oral squamous cell carcinoma (OSCC) to elucidate the relationship between Aurora-B expression and clinico-pathological findings by immunohistochemistry. Aurora-B expression was observed in normal oral squamous epithelia and OSCC cases, but the number of positive cells was significantly higher in OSCC than in normal squamous epithelium (p < 0.01). The labeling index of Aurora-B was significantly correlated with lymph node metastasis (p < 0.01) and histological grades of differentiation (p < 0.01). We also compared Aurora-B expression with Ki-67 expression and a positive correlation was found (p < 0.0001). Moreover, Aurora-B expression is significantly more frequent in multinuclear tumor cells than in total tumor cells. In summary, we found that Aurora-B expression was well correlated with cell proliferation, induction of multinuclear cells, histological differentiation, and metastasis in OSCC. These findings suggest that Aurora-B may be involved in tumor progression and that Aurora-B can be a new diagnostic and therapeutic target for OSCC.

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Section: Discussionmentioning

confidence: 99%

Aurora-B expression and its correlation with cell proliferation and metastasis in oral cancer

et al. 2007

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“…For examples, the p53 transcription factor directly binds the survivin promoter alone or in combination with other protein(s), such as E2F, Sin3 or HDAC, leading to the suppression of survivin (25,26). The p53 protein regulates survivin phosphorylation by binding to the subunit of Cdc2/cyclin B1 kinase (19), conversely, survivin could regulate p53 through caspase/Mdm2 (27) and Aurora B (28). Moreover, mutated p53 can stimulate the expression of survivin through one or more signaling pathways (29).…”

Section: Discussionmentioning

confidence: 99%

Epstein-Barr virus oncoprotein LMP1 mediates survivin upregulation by p53 contributing to G1/S cell cycle progression in nasopharyngeal carcinoma

Guo

Tang²,

Yang³

et al. 2012

International Journal of Molecular Medicine

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Latent membrane protein 1 (LMP1) is an important oncogenic protein encoded by Epstein-Barr virus (EBV) and plays an important role in the development of nasopharyngeal carcinoma (NPC). Our previous study has shown that p53 protein was accumulated and phosphorylated in NPC, implying its transcription factor activity in NPC tumorigenesis. However, the biological function and potential downstream target of p53 mediated by LMP1 in NPC remain unknown. In this study, we found that LMP1 simultaneously induced upregulation of both p53 and survivin at the protein level, as well as their phosphorylation. Knockdown of p53 by siRNA revealed that LMP1 increased survivin expression by p53 directly. Furthermore, we found that LMP1 upregulated survivin by p53 at the transcriptional level by increasing p53-mediated survivin promoter activity and DNA binding activity. Moreover, LMP1 induced the co-localization of p53 and survivin in the nucleus, conferring to their related functions in NPC tumorigenesis. We further found that p53 promoted G1/S cell cycle progression, but did not induce apoptosis in LMP1-positive NPC cells. Collectively, these findings suggest that p53 acting as a transcription factor promotes the transcriptional activity of survivin, and further increases its protein expression and phosphorylation in the regulation of LMP1, thus, leading to G1/S cell cycle progression with no effect on apoptosis in NPC tumorigenesis.

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“…Moreover, it was reported that the splic- ing variants of survivin which are currently identified by the anti-survivin antibodies due to the presence of an identical amino-terminal peptide in variants, may differ with the subcellular localization and functions in cell division and survival [23]. Aurora B kinase is over-expressed in several cancer types and there are some in vitro studies [35,43] that show the co-expression of survivin and Aurora B in various cell lines and tumors [44]. Although there was no published clinical study on correlation between survivin and Aurora B expression until recently, Qi G et al [30] showed a good association between nuclear survivin and Aurora B expression in head and neck squamous cell carcinoma.…”

Section: Discussionmentioning

confidence: 99%

High expression of nuclear survivin and Aurora B predicts poor overall survival in patients with head and neck squamous cell cancer

et al. 2012

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The negative prognostic values of high expression of Aurora B and high co-expression of nuclear survivin and Aurora B on survival were shown. These findings suggest that co-expression of nuclear survivin and Aurora B can be useful diagnostic markers and therapeutic targets for head and neck squamous cell carcinoma. However, further studies with a larger number of patients in a more homogeneous disease group are needed to confirm the conclusion.

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

Cited by 19 publications

References 29 publications

Aurora-B expression and its correlation with cell proliferation and metastasis in oral cancer

Aurora-B expression and its correlation with cell proliferation and metastasis in oral cancer

Epstein-Barr virus oncoprotein LMP1 mediates survivin upregulation by p53 contributing to G1/S cell cycle progression in nasopharyngeal carcinoma

High expression of nuclear survivin and Aurora B predicts poor overall survival in patients with head and neck squamous cell cancer

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