Knockout PTTG1 HCT116 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE58863 | GEO | 2015/11/23
SECONDARY ACCESSION(S): PRJNA253736
REPOSITORIES: GEO
Similar Datasets
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:RNA was extracted from cells using Aurum Total RNA kit from Bio-Rad Laboratories, Inc., Hercules, CA following the manufacturer’s recommendations. Gene expression profiling was performed using the BeadChip HumanHT-12 v4 Expression kit from Illumina®, which contains 47,231 gene-probes (Illumina® Inc., San Diego, CA). The raw signal intensities were imported and analyzed using the GenomeStudio® data software. After background subtraction and normalization, the signal intensity values were exported to the Partek® genomics expression analysis suite using “Partek's Report Plug-in” option in the GenomeStudio® software. Differentially expressed genes in the dox- versus vehicle-treated samples were identified using the “gene expression” workflow in the Partek® software.
2012-10-29 | GSE41894 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived HCT-116 cell transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis. Methods: HCT-116 cell mRNA profiles of HCT-116-GOLPH3-Vector and HCT-116-GOLPH3-Overepression were generated by deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Results: RNA sequencing (RNA-seq) was used to investigate gene expression in HCT-116-PMSCV-Vector and HCT-116-PMSCV GOLPH3 cells, while Gene Ontology (GO) was used to annotate the various functional genes. By comparing the differentially expressed genes, we noticed that GOLPH3 was associated with EMT. Gene set enrichment analysis (GSEA) analysis of the RNA-seq results based on the GSE77953 dataset was performed to investigate the biological functions of HCT-116-PMSCV-Vector and HCT-116-PMSCV-GOLPH3 cells. The findings suggested that GOLPH3 expression was positively associated with colon cancer cell autophagy. Signal pathway enrichment was next analyzed based on the differential expression of genes between HCT-116-PMSCV-Vector and HCT-116-PMSCV-GOLPH3 cells, as examined by RNA-seq. Notably, GOLPH3 has correlated with the PI3K/Akt signaling pathway. Conclusions: Our study represents the first detailed analysis of HCT-116 cell transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.
2022-02-23 | GSE196875 | 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.
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: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: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: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
2007-07-01 | GSE7447 | GEO
Project description:To identify the direct molecular targets of 6S, gene microarrays were used to profile gene expression in HCT-116 cells treated with 6S (20 uM for 24 h) comparing with HCT-116 cells treated with DMSO (control). Two-class comparisons. HCT-116 cells treated with 6S (20 uM for 24 h) vs. HCT-116 cells treated with DMSO control;Biological replicates: 4 replicates for each group.
2014-04-23 | E-GEOD-57006 | 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