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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Knockout PTTG1 HCT116 cells

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Yunguang Tong

PROVIDER: E-GEOD-58863 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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FoxM1 transactivates PTTG1 and promotes colorectal cancer cell migration and invasion.

Zheng Yun Y Guo Jinjun J Zhou Jin J Lu Jinjian J Chen Qi Q Zhang Cui C Qing Chen C Koeffler H Philip HP Tong Yunguang Y

BMC medical genomics 20150812

<h4>Background</h4>Metastasis is the major cause of cancer-related death. Forkhead Box M1 (FoxM1) is a master regulator of tumor metastasis. This study aims to identify new FoxM1 targets in regulating tumor metastasis using bioinformatics tools as well as biological experiments.<h4>Methods</h4>Illumina microarray was used to profile WT and PTTG1 knockout HCT116 cells. R2 Genomics Analysis was used to identify PTTG1 as a potential FoxM1 targeted gene. Luciferase reporter array, EMSA and Chromatin ...[more]

PMID: 26264222

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Knockout PTTG1 HCT116 cells

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

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Expression of PTTG1 is associated with aggressive clear cell RCC

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.

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Expression of PTTG1 is associated with aggressive clear cell renal carcinoma

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

Expression of PTTG1 is associated with aggressive clear cell renal carcinoma

2013-07-31 | E-GEOD-25493 | biostudies-arrayexpress

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