Human esophageal squamous cell carcinoma cell lines with downregulated PTTG1
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Fumiaki Sato
PROVIDER: E-GEOD-7447 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:To identify potential PTTG1-targeted genes, total RNA from PTTG1+/+ and PTTG1-/- HCT 116 cells was isolated using the RNeasy Kit (Qiagen) and analyzed using Illumina microarrays (HumanHT-12_V4). Raw data were processed according to the manufacturerâ??s standard procedure and further analyzed using Partek 6.5. PTTG1-/- and parent HCT116 cells. Experiment is performed in triplicate
2015-11-23 | E-GEOD-58863 | biostudies-arrayexpress
Project description:To identify potential PTTG1-targeted genes, total RNA from PTTG1+/+ and PTTG1-/- HCT 116 cells was isolated using the RNeasy Kit (Qiagen) and analyzed using Illumina microarrays (HumanHT-12_V4). Raw data were processed according to the manufacturer’s standard procedure and further analyzed using Partek 6.5.
2015-11-23 | GSE58863 | GEO
Project description:The pituitary-tumor transforming gene (PTTG1) is a recently discovered oncogene implicated in the malignant progression of a number of neoplasms. It has been shown to drive both endocrine and non-endocrine malignancies, but has not yet been studied in the context of renal cell carcinoma. Here we show that PTTG1 is frequently amplified and overexpressed in clear cell renal cell carcinoma, the most common form of kidney cancer. Clear cell RCC (ccRCC) is cytogenetically characterized by deletion of chromosome 3p, harboring the von-Hippel Lindau tumor suppressor gene, and amplification of chromosome 5q. The significance of copy number gain of chromosome 5 has to date remained a mystery, but is presumably the location of oncogenes that play an important role in ccRCC development or progression. The PTTG1 oncogene maps to chromosome 5q and shows frequent copy number gain in clear cell RCC, and is significantly overexpressed in tumor tissue relative to adjacent normal kidney. Furthermore, we have established a functional role for PTTG1 in ccRCC tumorigenesis and progression. PTTG1 ablation significantly reduces both the tumorigenic ability of ccRCC cells in vitro and in vivo and the invasive ability of these cells in vitro. An analysis of PTTG1 regulatory targets supports its role in the progression of localized ccRCC to invasive and metastatic disease, an idea further substantiated by PTTG1’s clinical correlation with high grade and high stage tumors and its association with poor prognosis. PTTG1-dependent overexpression of the Rho-GEF ECT2, another proto-oncogene, is observed in a number of ccRCC cell lines, and ECT2 overexpression correlates with PTTG1 overexpression, high stage, high grade, and poor prognosis in human ccRCC tumors. As GEF’s have been promoted as viable drug targets for targeted cancer therapeutics, the relationship between the PTTG1 and ECT2 oncogenes may be able to be exploited for the treatment of this disease. SNP data on 74 ccRCC and 16 normal renal tissue samples were used to profile the cytogenetic gains or losses. The most frequent gains or losses were identified and gene expression data were then used to pinpoint the genes for further study.
2010-12-31 | E-GEOD-25399 | biostudies-arrayexpress
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2013-07-01 | E-GEOD-44062 | biostudies-arrayexpress
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2014-08-01 | E-GEOD-44121 | biostudies-arrayexpress
Project description:The pituitary tumor-transforming gene (PTTG1) is a recently discovered oncogene implicated in the malignant progression of a number of neoplasms. It has been shown to drive both endocrine and non-endocrine malignancies, but has not yet been studied in the context of renal cell carcinoma (RCC). Clear cell RCC (ccRCC) is cytogenetically characterized by deletion of chromosome 3p, harboring the von-Hippel Lindau tumor suppressor gene, and amplification of chromosome 5q. The significance of copy number gain of chromosome 5 is not clear, but is presumed to be the location of oncogenes that influence ccRCC development or progression. The PTTG1 oncogene maps to chromosome 5q, and here we show that PTTG1 is amplified in clear cell RCC, is overexpressed in tumor tissue relative to adjacent normal kidney, and expression is associated with high grade, high stage, and poor prognosis. Furthermore, we establish a functional role for PTTG1 in ccRCC tumorigenesis and progression. PTTG1 ablation reduces both the tumorigenic ability of ccRCC cells in vitro and in vivo and the invasive ability of these cells in vitro. An analysis of genes whose transcription is regulated by PTTG1 was supportive of an association with invasive and metastatic disease. PTTG1-dependent expression of the Rho-GEF ECT2, another proto-oncogene, is observed in a number of ccRCC cell lines, and ECT2 expression correlates with PTTG1 expression, high stage, high grade, and poor prognosis ccRCC. As GEF's have been promoted as potential drug targets for targeted cancer therapeutics, the relationship between the PTTG1 and ECT2 oncogenes may be able to be exploited for the treatment of this disease. PTTG1 was knocked down by siRNA.
2013-07-31 | E-GEOD-25493 | biostudies-arrayexpress
Project description:The pituitary-tumor transforming gene (PTTG1) is a recently discovered oncogene implicated in the malignant progression of a number of neoplasms. It has been shown to drive both endocrine and non-endocrine malignancies, but has not yet been studied in the context of renal cell carcinoma. Here we show that PTTG1 is frequently amplified and overexpressed in clear cell renal cell carcinoma, the most common form of kidney cancer. Clear cell RCC (ccRCC) is cytogenetically characterized by deletion of chromosome 3p, harboring the von-Hippel Lindau tumor suppressor gene, and amplification of chromosome 5q. The significance of copy number gain of chromosome 5 has to date remained a mystery, but is presumably the location of oncogenes that play an important role in ccRCC development or progression. The PTTG1 oncogene maps to chromosome 5q and shows frequent copy number gain in clear cell RCC, and is significantly overexpressed in tumor tissue relative to adjacent normal kidney. Furthermore, we have established a functional role for PTTG1 in ccRCC tumorigenesis and progression. PTTG1 ablation significantly reduces both the tumorigenic ability of ccRCC cells in vitro and in vivo and the invasive ability of these cells in vitro. An analysis of PTTG1 regulatory targets supports its role in the progression of localized ccRCC to invasive and metastatic disease, an idea further substantiated by PTTG1’s clinical correlation with high grade and high stage tumors and its association with poor prognosis. PTTG1-dependent overexpression of the Rho-GEF ECT2, another proto-oncogene, is observed in a number of ccRCC cell lines, and ECT2 overexpression correlates with PTTG1 overexpression, high stage, high grade, and poor prognosis in human ccRCC tumors. As GEF’s have been promoted as viable drug targets for targeted cancer therapeutics, the relationship between the PTTG1 and ECT2 oncogenes may be able to be exploited for the treatment of this disease.
2010-12-31 | GSE25399 | GEO
Project description:The pituitary tumor-transforming gene (PTTG1) is a recently discovered oncogene implicated in the malignant progression of a number of neoplasms. It has been shown to drive both endocrine and non-endocrine malignancies, but has not yet been studied in the context of renal cell carcinoma (RCC). Clear cell RCC (ccRCC) is cytogenetically characterized by deletion of chromosome 3p, harboring the von-Hippel Lindau tumor suppressor gene, and amplification of chromosome 5q. The significance of copy number gain of chromosome 5 is not clear, but is presumed to be the location of oncogenes that influence ccRCC development or progression. The PTTG1 oncogene maps to chromosome 5q, and here we show that PTTG1 is amplified in clear cell RCC, is overexpressed in tumor tissue relative to adjacent normal kidney, and expression is associated with high grade, high stage, and poor prognosis. Furthermore, we establish a functional role for PTTG1 in ccRCC tumorigenesis and progression. PTTG1 ablation reduces both the tumorigenic ability of ccRCC cells in vitro and in vivo and the invasive ability of these cells in vitro. An analysis of genes whose transcription is regulated by PTTG1 was supportive of an association with invasive and metastatic disease. PTTG1-dependent expression of the Rho-GEF ECT2, another proto-oncogene, is observed in a number of ccRCC cell lines, and ECT2 expression correlates with PTTG1 expression, high stage, high grade, and poor prognosis ccRCC. As GEF's have been promoted as potential drug targets for targeted cancer therapeutics, the relationship between the PTTG1 and ECT2 oncogenes may be able to be exploited for the treatment of this disease.
2013-07-31 | GSE25493 | GEO
Project description:Meningiomas are frequent central nervous system tumors. Although most meningiomas are benign (WHO grade I) and curable by surgery, WHO grade II and III tumors remain therapeutically challenging due to frequent recurrence. Interestingly, relapse also occurs in some WHO grade I meningiomas. Hence, we investigated the transcriptional features defining aggressive (recurrent, malignantly progressing or WHO grade III) meningiomas in 144 cases. Meningiomas were categorized into non-recurrent (NR), recurrent (R), and tumors undergoing malignant progression (M) in addition to their WHO grade. Unsupervised transcriptomic analysis in 62 meningiomas revealed transcriptional profiles lining up according to WHO grade and clinical subgroup. Notably aggressive subgroups (R+M tumors and WHO grade III) shared a large set of differentially expressed genes (n=332; p<0.01, FC>1.25). In an independent multicenter validation set (n=82), differential expression of 10 genes between WHO grades was confirmed. Additionally, among WHO grade I tumors differential expression between NR and aggressive R+M tumors was af rmed for PTTG1, AURKB, ECT2, UBE2C and PRC1, while MN1 and LEPR discriminated between NR and R+M WHO grade II tumors. Univariate survival analysis revealed a significant association with progression-free survival for PTTG1, LEPR, MN1, ECT2, PRC1, COX10, UBE2C expression, while multivariate analysis identified a prediction for PTTG1 and LEPR mRNA expression independent of gender, WHO grade and extent of resection. Finally, stainings of PTTG1 and LEPR confirmed malignancy-associated protein expression changes. In conclusion, based on the so far largest study sample of WHO grade III and recurrent meningiomas we report a comprehensive transcriptional landscape and two prognostic markers. Comparative transcriptomic analysis of 62 low- and high-grade meningiomas
2016-02-15 | E-GEOD-74385 | biostudies-arrayexpress
Project description:The MicroArray Quality Control (MAQC) project was initiated to address these concerns, as well as other performance and analysis issues. We demonstrate the consistency of results within a platform across test sites as well as the high level of cross-platform concordance in terms of genes identified as differentially expressed. The MAQC study provides a rich resource that will help build consensus on the use of microarrays in research, clinical and regulatory settings. Manuscripts related to the MAQC project have been published in Nature Biotechnology, 24(9), September, 2006. More information about the MAQC project can be found at http://edkb.fda.gov/MAQC/.<br><br>Expression data from two distinct reference RNA samples (A and B) in four titration pools were generated at multiple test sites using a variety of microarray-based and alternative technology platforms. Sample A = Stratagene Universal Human Reference RNA (UHRR, Catalog #740000), Sample B = Ambion Human Brain Reference RNA (HBRR, Catalog #6050), Sample C = Samples A and B mixed at 75%:25% ratio (A:B); and Sample D = Samples A and B mixed at 25%:75% ratio (A:B). In general, each microarray platform was tested at three sites and each sample was tested in five replicates at each test site. Samples (hybridizations) were named according to the following convention: Platform_Testsite_SampleRelicate. For example, AFX_2_B1 represents the hybridization (array) from platform AFX processed by test site 2 for the first replicate of sample B. Assignment of platform code: ABI = Applied Biosystems (microarray); AFX = Affymetrix; AG1 = Agilent one-color; AGL = Agilent two-color; GEH = GE Healthcare; ILM = Illumina; NCI = NCI two-color (Operon oligos); EPP = Eppendorf; TAQ = TaqMan (Applied Biosystems); QGN = QuantiGene (Panomics); GEX = StaRT-PCR (Gene Express); H25K = TeleChem two-color; H25K1 = TeleChem one-color; BIO = CapitalBio two-color (Operon oligos); BIO1 = CapitalBio one-color (Operon oligos); OPN = Operon two-color (Operon oligos); NMC = Norwegian Microarray Consortium two-color (Operon oligos).
2006-12-04 | E-TABM-132 | biostudies-arrayexpress