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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Apoptosis gene signature of Survivin and its splice variant expression in breast carcinoma

ABSTRACT: Background: Survivin was described as strongly expressed in human cancer. To date, little is known about the association between Survivin splice variants and the other apoptosis-related genes. In this study, we analyzed the apoptosis gene signature of Survivin and its variant expression in breast cancer. Methods: Expression of the 5 transcripts was measured by RT-PCR in 135 breast carcinomas. Human Apoptosis Gene Arrays were used to screen the genes that could be associated with Survivin variants. Cox survival analysis was analyzed according to the breast cancer patient outcome. Results: Significant associations between Survivin transcript and the apoptotic gene array were found. Interestingly, Survivin-3B variant showed major inverse correlations with the pro-apoptotic gene array. Overexpression of Survivin-3B strongly inhibits 5-fluorouracil/epirubicin/Cyclophosphamide induced-apoptosis in breast tumor cell lines. In breast carcinomas, uni- and multivariate analysis showed patients with high level of survivin-3B expression had a shorter overall (p=0.030 and p=0.042, respectively) and disease-free (p=0.024 and p=0.009) survival. Conclusion: Our data indicate Survivin-3B could have an anti-apoptotic activity and its expression level might be used as a prognostic marker in breast carcinoma. The expression of 96 apoptosis genes and was analyzed in 41 breast carcinomas and 1 pool of normal mammary tissues. In parallel, every survivin isoform expression was quantified by real-time quantitative PCR. Data obtained with the macro-array were correlated with survivin isoform levels detected by RT-PCR.

ORGANISM(S): Homo sapiens

SUBMITTER: Romain Boidot

PROVIDER: E-GEOD-24556 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Apoptosis gene signature of Survivin and its splice variant expression in breast carcinoma

Project description:Background: Survivin was described as strongly expressed in human cancer. To date, little is known about the association between Survivin splice variants and the other apoptosis-related genes. In this study, we analyzed the apoptosis gene signature of Survivin and its variant expression in breast cancer. Methods: Expression of the 5 transcripts was measured by RT-PCR in 135 breast carcinomas. Human Apoptosis Gene Arrays were used to screen the genes that could be associated with Survivin variants. Cox survival analysis was analyzed according to the breast cancer patient outcome. Results: Significant associations between Survivin transcript and the apoptotic gene array were found. Interestingly, Survivin-3B variant showed major inverse correlations with the pro-apoptotic gene array. Overexpression of Survivin-3B strongly inhibits 5-fluorouracil/epirubicin/Cyclophosphamide induced-apoptosis in breast tumor cell lines. In breast carcinomas, uni- and multivariate analysis showed patients with high level of survivin-3B expression had a shorter overall (p=0.030 and p=0.042, respectively) and disease-free (p=0.024 and p=0.009) survival. Conclusion: Our data indicate Survivin-3B could have an anti-apoptotic activity and its expression level might be used as a prognostic marker in breast carcinoma.

2010-10-06 | GSE24556 | GEO

Transcription profiling of human MCF7 time-series upon RITA treatment.

Project description:Targeting “oncogene addiction” is a promising strategy for anti-cancer therapy. Here, we report a potent inhibition of crucial oncogenes by p53 upon reactivation with small molecule RITA in vitro and in vivo. RITA-activated p53 unleashes transcriptional repression of anti-apoptotic proteins Mcl-1, Bcl-2, MAP4, and survivin, blocks Akt pathway on several levels and downregulates c-Myc, cyclin E and B-catenin. p53 ablates c-Myc expression via several mechanisms at transcriptional and posttranscriptional level. We show that transrepression of oncogenes correlated with higher level of p53 bound to chromatin-bound p53 than transactivation of pro-apoptotic targets. Inhibition of oncogenes by p53 reduces the cell’s ability to buffer pro-apoptotic signals and elicits robust apoptosis. Our study highlights the role of transcriptional repression for p53-mediated tumor suppression. Experiment Overall Design: Breast carcinoma cell-line MCF7 was treated with the small-molecule p53 activator RITA for 2h, 8h, 16h and 24h.

2009-05-15 | E-GEOD-13291 | biostudies-arrayexpress

TEL-AML1 regulation of survivin and apoptosis via miRNA-494 and miRNA-320a

Project description:There is increasing evidence that microRNA and transcription factors interact in an instructive fashion in normal and malignant hematopoiesis. We explored the impact of TEL-AML1 (ETV6-RUNX1), the most common fusion protein in childhood leukemia, on miRNA expression and the leukemic phenotype. Using RNA interference, miRNA expression arrays, and quantitative PCR, we identified miRNA-494 and miRNA-320a to be upregulated upon TEL-AML1 silencing independently of TEL expression. Chromatin immunoprecipitation analysis identified miRNA-494 as a direct miRNA target of the fusion protein TEL-AML1. Using bioinformatic analysis as well as functional luciferase experiments we demonstrate that survivin is a target of the two miRNAs. MiRNA-494 and -320a were introduced to the cells by transfection and survivin expression determined by western blot analysis. These miRNAs blocked survivin expression and resulted in apoptosis in a similar manner as TEL-AML1 silencing by itself; this silencing was also shown to be DICER-dependent. MiRNAs-494 and -320a are expressed at lower levels in TEL-AML1+ leukemias compared to immunophenotype-matched non-TEL-AML1 ALL subtypes, and within TEL-AML1+ leukemias their expression is correlated to survivin levels. In summary our data suggest that TEL-AML1 might exert its anti-apoptotic action at least in part by suppressing miRNA-494 and miRNA-320a, lowering their expression causing enhanced survivin expression. DNAs from REH cells were pulled down using ChIP antibodies to TEL and hybridized to microRNA promoter tiling arrays.

2010-08-28 | E-GEOD-23842 | biostudies-arrayexpress

Homo sapiens

Project description:Apoptosis gene signature of Survivin and its splice variant expression in breast carcinoma

| PRJNA132621 | ENA

Survivin deficient liver of mice after partial hepatectomy

Project description:The liver possesses remarkable regenerative capacity in response to injury. Upon partial hepatectomy (PHx), terminally differentiated hepatocytes in the remaining liver enter the cell cycle and restore the liver mass and function within weeks. However, liver regeneration is often impaired in livers with chronic diseases. Survivin, an inhibitor of apoptosis protein (IAP) and member of chromosome passenger complex (CPC), plays versatile roles in cell mitosis and apoptosis. We and others found that the expression of Survivin was highly increased in liver during PHx-induced liver regeneration, which indicated that Survivin played important roles in this process. However, the function of Survivin in liver regeneration remains largely undefined. Here, using mice with genetic deletion of Survivin, we found that during PHx-induced liver regeneration Survivin regulated both hepatocyte G1/S phase transition by inhibiting the expression of p21 and G2/M phase transition by regulating the localization of CPC. Moreover, restoration of Survivin expression in Survivin-deficient hepatocytes inhibited p21 expression and promote both hepatocyte G1/S and G2/M transition during PHx-induced liver regeneration.

2017-01-01 | GSE83598 | GEO

TEL-AML1 regulation of survivin and apoptosis via miRNA-494 and miRNA-320a

2010-08-28 | GSE23842 | GEO

MCF7 time-series upon RITA treatment.

2009-05-12 | GSE13291 | GEO

Survivin deficient Hepatocellular carcinoma and non-cancerous tissue of mice

Project description:Hepatocellular carcinoma (HCC) is a deadly cancer lacking efficacious therapies. Latest studies show that cellular senescence and inflammation play key roles in HCC development, likely reflecting its etiological nature of chronic infection. A better understanding of these intertwined processes would facilitate development of therapies for malignant HCCs. Here, we show that malignant HCCs are drastically reduced after deletion of Survivin, an inhibitor of apoptosis protein. Survivin deficiency induces mitosis defect-caused metabolism reprogram and senescence in HCC cells. Survivin additionally protects both senescent and neighboring non-senescent cancer cells from cell death triggered by senescence-associated inflammatory factor TNFα. Importantly, combination of mitosis inhibitor and pro-apoptosis drug, but not alone, synergistically eliminates HCCs, recapitulating the therapeutic effect of genetic deletion of Survivin. By uncovering the role of Survivin in controlling the interaction of senescence and inflammation responses, our findings propose a strategy for HCC therapy by inducing senescence and boosting TNFα-mediated cell death.

2016-06-22 | GSE64804 | GEO

Transcription profiling of pancreatic islet implanted transgenic (expressing survivini) in mice

Project description:Transgenic mice were generated that expressed the inhibitor of apoptosis and mitotic regulator survivin in pancreatic islet beta cells. Control non-transgenic or transgenic islets were then used in a model of islet transplantation in diabetic recipient mice and tested for their ability to correct hyperglycemia and allow long-term engraftment of tranplanted islets in vivo. Control or transgenic islets were analyzed by chip microarray for potential transcriptional changes associated with transgenic expression of survivin, in vivo.

2006-01-16 | E-MEXP-536 | biostudies-arrayexpress

Mesalazine for the prevention of colorectal cancer: effects in patients with a history of sporadic adenomatous polyps

Project description:Primary objectives: Identify chemopreventive properties of mesalazine in patients at high risk of recurrent (nonfamilial) colorectal adenomas by evaluating the effect of treatment on apoptosis and proliferation in histologically normal sigmoid and rectal mucosa relative to the placebo group. Primary endpoints: The effect of treatment with mesalazine on apoptotic and proliferation indices relative to the placebo group.

| 2529518 | ecrin-mdr-crc

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