Inhibitor of apoptosis protein (IAP) survivin is upregulated by oncogenic c-H-Ras

Sommer, Klaus W.; Schamberger, Chantal; Schmidt, Gerlinde; Sasgary, Soleman; Cerni, Christa

doi:10.1038/sj.onc.1206509

Cited by 90 publications

(80 citation statements)

References 63 publications

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“…11,35 The latter finding is consistent with the fact that 90% of SCLC tumors and almost all cell lines have mutations in p53. 2,36 In addition, we show that in SCLC cells survivin is modulated by the PI3K/Akt pathway that has emerged as a frequently activated survival pathway in various cancer types.…”

Section: Discussionsupporting

confidence: 80%

Cisplatin activates Akt in small cell lung cancer cells and attenuates apoptosis by survivin upregulation

Belyanskaya¹,

Hopkins-Donaldson²,

Kurtz³

et al. 2005

Intl Journal of Cancer

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The inhibitor of apoptosis protein (IAP) survivin is overexpressed in many tumors but is absent in most normal adult tissues. We report high levels of survivin expression in small cell lung cancer (SCLC), and describe the role of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in survivin upregulation. Moreover, the cytoprotective function of survivin in response to the anti-cancer agent cisplatin (CDDP) was investigated. Negative modulation of PI3K/ Akt using pharmacological inhibitors or dominant negative Akt (DN-Akt) decreased Akt kinase activity and resulted in decreased survivin expression and phosphorylation on Thr34, whereas transfection of constitutively active Akt (CA-Akt) increased survivin expression and phosphorylation. Interestingly, we found that treatment of SCLC cells with CDDP further increased survivin expression in a cell cycle independent manner by activation of Akt. CA-Akt or lentiviral survivin also inhibited apoptosis induced by CDDP, whereas DN-Akt or survivin-specific RNA interference sensitized cells to CDDP. We identified survivin as an anti-apoptotic protein in SCLC cells that is regulated by Akt, and demonstrate that treatment with the DNA damaging agent CDDP activates the PI3K/Akt/survivin pathway that in part protects cells from drug-induced apoptosis. ' 2005 Wiley-Liss, Inc.

show abstract

Section: Discussionsupporting

confidence: 80%

Cisplatin activates Akt in small cell lung cancer cells and attenuates apoptosis by survivin upregulation

Belyanskaya¹,

Hopkins-Donaldson²,

Kurtz³

et al. 2005

Intl Journal of Cancer

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“…Previous studies showed that, ectopic overexpression of c-H-Ras in rat cells as well as in human keratinocytes induces survivin expression. 13,14 Furthermore, Fukuad et al showed that exogenous H-Ras is required for interleukin induced survivin in Baf-3 cells. 15 However, other studies showed that mutant H-Ras is not able to increase survivin.…”

Section: Introductionmentioning

confidence: 99%

Depletion of K-Ras promotes proteasome degradation of survivin

Tecleab

Sebti²

2013

Cell Cycle

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“…It enters cells under the stimulation of the Fas gene and cell proliferation, wherein it binds the cyclin CDK4, leading to CDK2/cyclin E activation and Rb phosphorylation. These processes promote DNA replication and shorten the G1/S course (Sommer et al, 2003). Furthermore, the formation of the survivin/CDK4 complex allows p21waf1/cip1 to be released from the p21waf1/cip1-CDK4 complex.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of survivin-targeting small interfering RNA on gastric cancer cells

Chen

Zhang

et al. 2014

Genet. Mol. Res.

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ABSTRACT.A pair of inverted repeated sequences of the gene survivin was designed for stable double-stranded RNA establishment. After stable transfection, the biological behaviors of gastric cancer cells were observed. The interference rates of survivin-targeting siRNA (siRNA-survivin) in BGC823, MKN45, SGC7901, and cisplatin-resistant SGC7901 groups were 55.363 ± 3.974, 71.433 ± 3.774, 69.433 ± 7.336, and 76.767 ± 3.541%, respectively, compared with those in the control group. After siRNA-survivin interference, survivin protein expression noticeably decreased, apoptotic rates markedly increased, and cell proliferation was inhibited to varying degrees. Mitochondrial cytochrome C protein expression decreased and the levels of cytoplasmic cytochrome C and caspase-3 increased, which showed significant differences compared with values before transfection. pRNA-shSU eukaryotic expression vectors were constructed. After plasmid transfection, green fluorescent protein expression increased and survivin protein expression noticeably increased in BGC823 and SGC7901. siRNA-survivin promotes GC cell apoptosis and inhibits cell proliferation by downregulating survivin mRNA and protein expression. The underlying mechanisms 6787 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (3): 6786-6803 (2014) siRNA-survivin inhibits gastric cancer cell growth are correlated with a decrease in mitochondrial cytochrome C and cytoplasmic cytochrome C and caspase-3.

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Inhibitor of apoptosis protein (IAP) survivin is upregulated by oncogenic c-H-Ras

Cited by 90 publications

References 63 publications

Cisplatin activates Akt in small cell lung cancer cells and attenuates apoptosis by survivin upregulation

Cisplatin activates Akt in small cell lung cancer cells and attenuates apoptosis by survivin upregulation

Depletion of K-Ras promotes proteasome degradation of survivin

Inhibitory effect of survivin-targeting small interfering RNA on gastric cancer cells

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