Transforming properties of 8p11-12 amplified genes in human breast cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE23734 | GEO | 2010/08/21
SECONDARY ACCESSION(S): PRJNA130791
REPOSITORIES: GEO
Similar Datasets
Project description:Amplification of the 8p11-12 region has been found in about 15% of human breast cancers and is associated with poor prognosis. Earlier, we used genomic analysis of copy number and gene expression to perform a detailed analysis of the 8p11-12 amplicon to identify candidate oncogenes in breast cancer. We identified 21 candidate genes and provided evidence that three genes, namely, LSM-1, TC-1, and BAG4, have transforming properties when overexpressed. In the present study, we systematically investigated the transforming properties of 13 newly identified 8p11-12 candidate oncogenes in vitro. WHSC1L1, DDHD2, and ERLIN2 were most potently transforming oncogenes based on the number of altered phenotypes expressed by the cells. WHSC1L1 contains a PWWP-domain that is a methyl-lysine recognition motif involved in histone code modification and epigenetic regulation of gene expression. Knockdown of WHSC1L1 in 8p11-12-amplified breast cancer cells resulted in profound loss of growth and survival of these cells. Further, we identified several WHSC1L1 target genes, one of which is iroquois homeobox 3 gene (IRX3), a member of the Iroquois homeobox transcription factor family.
| S-EPMC3089754 | biostudies-literature
Project description:Total RNA was isolated from SUM-44 cells subjected to 5 days of puromycin selection following infection with lentiviral shRNA constructs against NSD3-S or ESR1 as well as LacZ control. Samples were harvested in triplicate and prepared and sequenced simultaneously.
2018-09-01 | E-MTAB-5823 | biostudies-arrayexpress
Project description:RNA-seq of MCF10A transduced with an inducible lentiviral MYB expression system
| PRJEB62551 | ENA
Project description:This analysis was performed with the aim of finding the genes differentially expressed in fibroblasts transduced with the E6/E7 genes of HPV 16, 18, 38b, 107 and 122. The name given for the samples are as follows: FB-E6E7-16, FB-E6E7-18, FB-E6E7-38b, FB-E6E7-107, FB-E6E7-122, and for fibroblasts transduced with the empty lentiviral vector pLVX, they were referred as FB-pLVX. Methods: Library construction and Illumina NovaSeq 6000 sequencing was performed by Novogene Bioinformatics Technology Co., Ltd, Beijing, China, on HPV 16, 18, 38b, 107 and 122 E6E7 Transduced Fibroblasts; three independently mRNA sequences were performed for each of the cell models. Bioinformatics analyses were performed as follows: raw reads were analyzed using the open source Galaxy platform (https://www.usegalaxy.org) and RStudio software (2021.09.0). The quality of the reads was checked using the FastQC tool, and the Trimmomatic tool was used to remove ambiguous nucleotides. Subsequently, all clean reads were mapped to the human genome reference (hg38 vs 38) using Rsubread for RStudio. Once all BAM files were obtained, reads were counted using the featureCounts tool, and gene expression analysis was performed using the DESeq2 tool. The gene expression level was normalized using the fragments per kilobase of transcript per million mapped reads (FPKM) method. Data validation was performed by real-time PCR. Conclusions: Our study represents the first analysis of genes differentially expressed by the E6/E7 proteins of HPV genus Beta-2 (38b, 107 and 122), through RNA-seq technology. This study shows the transforming potential that genotypes of the Beta-2 genus, especially HPV122, also possess. These Beta-2 HPVs can modulate some of the genes that are well known to be regulated by Alpha-HPVs 16 and 18.
2022-07-21 | GSE191090 | GEO
Project description:HER2 transduced cells which we will refer to as HER2-DOX –. These cells are 99% GFP positive (i.e., 99% cells have HER2 transduced, un-induced). As a control, we had GFP empty vector transduced MCF10A cells (95% have GFP transduced). Both cell types in triplicates. We had 4 time-points 0h, 30 mins, 4hours, and 7 hours (time duration for which HER2 will be induced). DOX was added to the GFP-MCF10A cells as a control. Only 1ug/ml of DOX was be used.
2023-01-23 | PXD034105 | Pride
Project description:The first bona fide PTP proto-oncogene was the Src-homology 2 domain-containing phosphatase SHP2 (encoded by PTPN11), an ubiquitously expressed PTP that transduces mitogenic, pro-survival, cell fate and/or pro-migratory signals from numerous growth factor-, cytokine- and extracellular matrix receptors. In malignancies, SHP2 is hyperactivated either downstream of oncoproteins or by mutations.We provide analysis of the mammary epithelial cells MCF10A overexpressing human HER2 and HER3 and grown in 3D cultures for 15 days in the presence or absence of SHP2. The human mammary epithelial cells MCF10A were transduced with a doxycycline-inducible lentiviral vector expressing a CTRL miR or SHP2 miR1 or SHP2 miR2. Cells from each group were grown in 3D cultures, and the knockdown of SHP2 was induced for 15 days. RNA was extracted for gene expression analysis.
2011-12-20 | E-GEOD-34524 | biostudies-arrayexpress
Project description:Genetic and epigenetic (DNA methylation, histone modifications, microRNA expression) crosstalk promotes inactivation of tumor suppressor genes or activation of oncogenes by gene loss/hypermethylation or duplications/hypomethylation, respectively. The 8p11-p12 chromosomal region is a hotspot for genomic aberrations (chromosomal rearrangements, amplifications and deletions) in several cancer forms, including breast carcinoma where amplification has been associated with increased proliferation rates and reduced patient survival. Here, an integrative genomics screen (DNA copy number, transcriptional and DNA methylation profiling) performed in 229 primary invasive breast carcinomas identified substantial coamplification of the 8p11-p12 genomic region and the MYC oncogene (8q24.21), as well as aberrant methylation and transcriptional patterns for several genes spanning the 8q12.1-q24.22 genomic region (ENPP2, FABP5, IMPAD1, NDRG1, PLEKHF2, RRM2B, SQLE, TAF2, TATDN1, TRPS1, VPS13B). Taken together, our findings suggest that MYC activity and aberrant DNA methylation may also have a pivotal role in the aggressive tumor phenotype frequently observed in breast carcinomas harboring 8p11-p12 regional amplification.
| S-EPMC4038389 | biostudies-literature
Project description:Mesoangioblasts are vessel-associated progenitor cells that show therapeutic promise for the treatment of muscular dystrophy. Mesoangioblasts have the ability to undergo skeletal muscle differentiation and cross the blood vessel wall regardless of the developmental stage at which they are isolated. Here we show that PW1/Peg3 is expressed at high levels in mesoangioblasts obtained from mouse, dog and human tissues and its level of expression correlates with their myogenic competence. Silencing PW1/Peg3 markedly inhibits myogenic potential of mesoangioblasts in vitro through MyoD degradation. Moreover, lack of PW1/Peg3 abrogates mesoangioblast ability to cross the vessel wall and to engraft into damaged myofibers through the modulation of the junctional adhesion molecule-A. We conclude that PW1/Peg3 function is essential for conferring proper mesoangioblast competence and that the determination of PW1/Peg3 levels in human mesoangioblasts may serve as a biomarker to identify the best donor populations for therapeutic application in muscular dystrophies. Ctrl Mesoangioblasts (MABs) transduced with a Lentiviral vector shControl (2 replicates, Ctrl_1 and Ctrl_2) and shPW1 Mesoangioblasts transduced with a Lentiviral vector shPW1 (2 replicates, PW1-siRna_1 and PW1-siRna_2)
2015-01-19 | E-GEOD-64334 | biostudies-arrayexpress
Project description:Improved understanding of mechanisms regulating myelodysplastic syndrome (MDS) hematopoietic stem/progenitor cell (HSPC) growth and self-renewal is critical for developing MDS therapy. We revealed a novel regulatory axis that SIRT1-deficiency induced TET2 hyperacetylation promotes MDS HSPC functions, and provide an approach to target MDS HSPCs by activating SIRT1 deacetylase. Four Groups: Group1: MDS-L cells transduced with lentiviral vector targeting non-silence squence (control shRNA for SIRT1); Group2: MDS-L cells transduced with lentiviral vector containing interference squence targeting SIRT1 (SIRT shRNA); Group 3: MDS-L cells transduced with lentiviral vector targeting non-silence squence (control shRNA for TET2); Group 4: MDS-L cells transduced with lentiviral vector containing interference squence targeting TET2 (TET2 shRNA).
2018-08-13 | GSE117272 | GEO
Project description:Comparative analysis of the transcriptome of 4T1 cells stably transduced with a lentiviral vector expressing a siRNA against murine SPARC (4T1-C18) with 4T1 control cells stably transduced with a lentiviral vector expressing a scramble sequence (4T1-SCR).
2016-06-29 | GSE83830 | GEO