Human esophageal squamous cell carcinoma cell lines with downregulated PTTG1
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE7447 | GEO | 2007/07/01
SECONDARY ACCESSION(S): PRJNA100221
REPOSITORIES: GEO
Similar Datasets
Project description:We conducted a comprehensive genome-wide interrogation to identify gene targets regulated by PTTG1 using a bead-array platform. The raw data and normalized logarithmic data were included in this subset. Keywords: siRNA, esophageal cells HSA/c and KYSE140 cells were transfected with three siRNA oligos (NTC, P1, P2) separately or without oligos (LF+) at day 0 and harvested at day 3. Total RNAs were extracted by the RNeasy kit (Qiagen) from the eight samples. After the RNA quality measurement by the Bioanalyzer 2100 (Agilent Technologies, Santa Clara, CA), each RNA sample (100 ng) was amplified with the Illumina TotalPrep RNA Amplification kit (Ambion, Austin, TX), hybridized with the Illumina Human RefSeq8 version 2 BeadChip with 20,589 transcript probes comprised of optimized 50 mer-oligonucleotides (Illumina, San Diego, CA), washed, and stained with Cy3-streptavidin (GE Healthcare) as per the manufacturesâ instructions. The arrays were scanned with the Illumina Beadarray Reader confocal scanner (Illumina) and the data were processed using the Illumina BeadStudio software (Illumina). The data were subjected to intensity-dependent normalization, and differentially expressed genes by PTTG1 downregulation were identified by the Significance Analysis of Microarrays (SAM) program.
2010-06-10 | E-GEOD-7447 | biostudies-arrayexpress
Project description:Esophageal squamous cell carcinoma (ESCC) is the major histological type of esophageal cancers worldwide. Transcription factor PTTG1 was seen highly expressed in a variety of tumors and was related to the degree of tumor differentiation, invasion, and metastasis. However, the clinical significance of PTTG1 had yet to be verified, and the mechanism of abnormal PTTG1 expression in ESCC was not clear. In this study, we collected eight pairs of ESCC samples and corresponding adjacent normal esophageal tissues for RNA-seq from eight ESCC patients underwent radical resection of EC. None of these ESCC patients received preoperative chemotherapy or radiotherapy.The tissue samples were stored at -80°C immediately after resection. These 8 patients included 6 males and 2 females with a median age of 60 years. RNA-seq was executed by Wuhan Seqhealth Technology Co.LTD. TRIzol reagent (Invitrogen, Carlsbad, CA, USA) was applied to extract and prepare total RNA from tumors and paired adjacent non-ESCC tissues. A total amount of 3 μg RNA per sample was used as initial material for the RNA sample preparations. Nanodrop™ 1000 spectrophotometer was applied to examined RNA purity. RNA concentration was determined using a Qubit® 3.0 Fluorometer. RNA integrity was determined using an RNA Nano 6000 Assay Kit and a Bioanalyzer 2100 system. Afterward, the sequencing libraries were established using the NEBNext Ultra Directional RNA Library Prep Kit for Illumina base on manufacturer’s protocols. The 200 Illumina HiSeq X Ten platform was used to sequence the libraries. RNA sequencing reads were aligned to the reference of homo_sapiens.GRCh38. In the current study, we obtained the data on log2 (x + 0.001) conversion level 3 and reported RNA-seq data in transcripts per kilobase million (TPM).
2021-01-17 | GSE164158 | GEO
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: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:The clinical significance and potential molecular mechanism of PTTG1 in esophageal squamous cell carcinoma
| PRJNA689307 | ENA
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:Background & Aims: Esophageal squamous cell carcinoma (ESCC) is believed to arise from esophageal mucosa through accumulation of both genetic and epigenetic changes. DNA methylation is a critical epigenetic mechanism involved in key cellular processes and its deregulation has been linked to many human cancers, including ESCC. The aim of this study is to examine the global deregulation of methylation states in ESCC and identify potential early biomarkers. Conclusions: This is the first study to address methylation changes in ESCC in a large panel of genes. Methylome analysis is shown as a sensitive and powerful tool to identify molecular players in ESCC. These data should prove to be the reference for future studies identifying potential biomarkers and molecular targets of ESCC. We performed a bead array analysis of more than 800 cancer-related genes in a series of 10 ESCC samples, 10 matched surrounding tissues, and 4 esophageal mucosa from healthy individuals. Pyrosequencing was used for validation of DNA methylation changes in up to 106 patients and 27 controls.
2011-11-23 | E-GEOD-26784 | 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.
2013-07-31 | GSE25493 | 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. 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. 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