Survivin initiates procaspase 3/p21 complex formation as a result of interaction with Cdk4 to resist Fas-mediated cell death

Suzuki, Atsushi; Ito, Takeshi; Kawano, Hirokazu; Hayashida, Midori; Hayasaki, Yayoi; Tsutomi, Yumi; Akahane, Kouichi; Nakano, Takeshi; Miura, Masayuki; Shiraki, Katsuya

doi:10.1038/sj.onc.1203429

Cited by 224 publications

(158 citation statements)

References 37 publications

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“…Our study has confirmed that EBV LMP1 could cause the G 1 /S check point disorder and accelerate G 1 -S transition in NPC cells [15,16]. G 1 /S check point is a critical restriction point co-regulated by Cyclin D and CDK4.…”

Section: Initiation Of Survivin/ Cdk4 Complex Formation In the Nucleisupporting

confidence: 74%

“…Meanwhile, Suzuki reported that Survivin could promote cell proliferation by competitively interacting with CDK4, over-expression of Survivin could release CDK inhibitors p21 (WAF1/Cip1) and p16 INK4a from CDK4. This molecular interaction may play an important role in carcinogenesis and progression of human HCC [15][16]. Therefore, detailed mechanism of LMP1 regulating Survivin in G 1 /S phase need to be further confirmed.…”

Section: Introductionmentioning

confidence: 98%

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Regulation of Survivin and CDK4 by Epstein-Barr virus encoded latent membrane protein 1 in nasopharyngeal carcinoma cell lines

Zhao

et al. 2005

Cell Res

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Latent membrane protein 1 (LMP1), an important protein encoded by Epstein Barr virus (EBV), has been implied to link with the pathogenesis of nasopharyngeal carcinoma (NPC). Its dual effects of increasing cell proliferation and inhibiting cell apoptosis have been confirmed. In this study, we showed that the expression of Survivin and CDK4 protein in CNE-LMP1, a LMP1 positive NPC epithelial cell line, is higher than in LMP1 negative NPC epithelial cell line-CNE1, and the expression is LMP1 dosage-dependent. Although it was reported that Survivin specifically expressed in cell cycle G 2 /M phase, our studies suggested that LMP1 could promote the expression of Survivin in G 0 /G 1 , S and G 2 / M phase. It also showed that Survivin and CDK4 could be accumulated more in the nuclei triggered by LMP1. More interestingly, Survivin and CDK4 could form a protein complex in the nuclei of CNE-LMP1 rather than in that of CNE1, which demonstrated that the interaction between these two proteins could be promoted by LMP1. These results strongly suggested that the role of LMP1 in the regulation of Survivin and CDK4 may also shed some light on the mechanism research of LMP1 in NPC.

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Section: Initiation Of Survivin/ Cdk4 Complex Formation In the Nucleisupporting

confidence: 74%

Section: Introductionmentioning

confidence: 98%

Regulation of Survivin and CDK4 by Epstein-Barr virus encoded latent membrane protein 1 in nasopharyngeal carcinoma cell lines

Zhao

et al. 2005

Cell Res

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“…43 However, the mechanisms of apoptotic suppression by survivin are not completely clear. Initial observations suggested that survivin could directly suppress activation of caspase-3 44,45 ; however, more recent studies have demonstrated that survivin lacks the ability to directly inhibit caspase-3. 46,47 Other groups have proposed that survivin acts like other IAPs by binding to caspase-9 and/or by neutralizing the new IAP-inhibiting protein, Smac/Diablo, 48,49 raising the possibility that it might suppress caspases indirectly by freeing other IAP family members from the constraints of this protein.…”

Section: Discussionmentioning

confidence: 99%

Nuclear Survivin Expression in Mantle Cell Lymphoma Is Associated with Cell Proliferation and Survival

Martı́nez

Bellosillo

Bosch

et al. 2004

The American Journal of Pathology

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Survivin is a member of the inhibitor of apoptosis protein family that is expressed inMantle cell lymphoma (MCL) is a malignant lymphoproliferative disorder characterized by the proliferation of CD5ϩ, CD23-monoclonal B cells containing the chromosomal translocation t(11;14)(q13;q32) which places the cyclin D1 gene under the transcriptional control of the immunoglobulin heavy chain enhancer elements.

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“…These observations indicate that survivin may have an important role in the progression of HCCs. 16 Although it has been demonstrated that interference with survivin expression or function could inhibit the neoplastic growth of a wide variety of cancers, to date, there are still few reports to experimentally support this theory in HCC. 17 We reasonably postulate that survivin may be a promising and powerful target for the treatment of HCC.…”

Section: Introductionmentioning

confidence: 99%

Survivin knockdown by short hairpin RNA abrogates the growth of human hepatocellular carcinoma xenografts in nude mice

Zhang

Zheng

et al. 2009

Cancer Gene Ther

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Abnormal high activation of survivin is involved in carcinogenesis of various types of cancer. Survivin has been shown to promote cell proliferation in human hepatocellular carcinoma (HCC). Survivin-targeting approaches have become a promising strategy for treating HCC. Here, we used a reporter system to screen effective survivin siRNA sequences. The effect of vector-based survivin short hairpin RNA (shRNA) on the malignant phenotype of HCC cells in vitro and in vivo was determined, and an adenovirusmediated shRNA expression vector was developed to decrease survivin expression of the established HCC tumor in nude mice. In vitro study showed that stable survivin knockdown inhibited cancer cell proliferation, enhanced apoptotic susceptibility, arrested cell cycle in the G1 phase and resulted in apparent mitotic catastrophe. Moreover, cells stably expressing survivin shRNA showed decreased tumorigenicity in nude mice. An additional in vivo study showed that intratumoral injection of adenovirus-delivered survivin shRNA suppressed tumor growth by spontaneous apoptosis of cancer cells and significantly prolonged animal survival. In conclusion, we proved the therapeutic potential of survivin shRNA for the treatment of HCC. And our results indicated that adenovirus-delivered shRNA may serve as a novel therapeutic for HCC.

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Survivin initiates procaspase 3/p21 complex formation as a result of interaction with Cdk4 to resist Fas-mediated cell death

Cited by 224 publications

References 37 publications

Regulation of Survivin and CDK4 by Epstein-Barr virus encoded latent membrane protein 1 in nasopharyngeal carcinoma cell lines

Regulation of Survivin and CDK4 by Epstein-Barr virus encoded latent membrane protein 1 in nasopharyngeal carcinoma cell lines

Nuclear Survivin Expression in Mantle Cell Lymphoma Is Associated with Cell Proliferation and Survival

Survivin knockdown by short hairpin RNA abrogates the growth of human hepatocellular carcinoma xenografts in nude mice

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