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Differentiation resistant HPV16-immortalized keratinocytes: Six1 transfected vs. Control.

ABSTRACT: The overexpression of Six1, a member of the Six family of homeodomain transcription factors, has been found in various human cancers, and is associated with tumor progression and metastasis. We previously determined that the expression of Six1 mRNA increased during in vitro progression of human papillomavirus type 16 (HPV16)-immortalized human keratinocytes (HKc/HPV16) toward a differentiation-resistant (HKc/DR) phenotype. However, if Six1 promotes HPV16-mediated transformation or not remains unknown. HKc/DR were transfected with a Six1 or control vector and RNA isolated from these cells were used in an Agilent two-color gene expression profiling experiment. The goal was to determine the effects of Six1 on global gene expression. Two-condition experiment, Six1 vs. Control HKc/DR cells. Biological replicates: 4 Six1-transfected replicates and 4 control-transfected replicates.

ORGANISM(S): Homo sapiens

SUBMITTER: Kim Creek

PROVIDER: E-GEOD-53589 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Differentiation resistant HPV16-immortalized keratinocytes: Six1 transfected vs. Control.

Project description:The overexpression of Six1, a member of the Six family of homeodomain transcription factors, has been found in various human cancers, and is associated with tumor progression and metastasis. We previously determined that the expression of Six1 mRNA increased during in vitro progression of human papillomavirus type 16 (HPV16)-immortalized human keratinocytes (HKc/HPV16) toward a differentiation-resistant (HKc/DR) phenotype. However, if Six1 promotes HPV16-mediated transformation or not remains unknown. HKc/DR were transfected with a Six1 or control vector and RNA isolated from these cells were used in an Agilent two-color gene expression profiling experiment. The goal was to determine the effects of Six1 on global gene expression.

2013-12-24 | GSE53589 | GEO

Expression data from SIX1 knocked-down HKc/DR cells

Project description:The homeodomain transcription factor SIX1 plays a critical role in embryogenesis, is not expressed in normal adult tissue, but is expressed in many malignancies, including cervical cancer. SIX1 drives the progression of HPV16-immortalized human keratinocytes (HKc/HPV16) toward malignancy: HKc/HPV16 express high levels of SIX1 mRNA and protein; overexpression of SIX1 in HKc/HPV16 produces pre-malignant, differentiation-resistant lines (HKc/DR); SIX1 overexpression in HKc/DR induces tumorigenicity. In this paper, we explore the consequences of inhibition of SIX1 expression in premalignant HKc/DR. Only partial inhibition of SIX1 expression could be obtained in HKc/DR by RNA interference. Decreased SIX1 expression (up to 80%) in HKc/DR resulted in slower proliferation, decreased HPV16-E6/E7 mRNA levels, and increased p53 protein levels. Gene expression changes induced in HKc/DR by anti-SIX1 shRNA were indicative of mesenchymal-epithelial transition (EMT) and changes in TGF-beta signaling. We conclude that HPV16-transformed cells depend on SIX1 for survival, continuous HPV16 E6/E7 gene expression and EMT.

2019-08-20 | GSE126926 | GEO

Homo sapiens

Project description:Differentiation resistant HPV16-immortalized keratinocytes: Six1 transfected vs. Control.

| PRJNA232462 | ENA

MLL Fusion Proteins Preferentially Regulate a Small Set of Wild Type MLL Target Genes in the Leukemic Genome

Project description:MLL encodes a histone methyltransferase that is critical in maintaining gene expression during embryonic development and hematopoiesis. 11q23 translocations encode chimeric MLL fusions that act as potent drivers of acute leukemia. However, it remains unclear what portion of the leukemic genome is under the direct control of the MLL fusion protein. By comparing patient-derived leukemic cell lines, we find that MLL fusion-bound genes are a small subset of that recognized by wild-type MLL. In an inducible MLL-ENL cellular model, binding of the MLL fusion protein and changes in H3K79 methylation are limited to a specific portion of the genome, whereas wild-type MLL distributes to a much larger set of gene loci. Surprisingly, among 223 MLL fusion-bound genes, only 12 demonstrate a significant increase in mRNA expression upon induction of the fusion protein. In addition to Hoxa9 and Meis1, this includes Eya1 and Six1 which comprise a heterodimeric transcription factor important in several developmental pathways. We show that Eya1 has the capacity to immortalize hematopoietic progenitor cells in vitro and collaborates with Six1 in hematopoietic transformation assays. Altogether, our data suggest that MLL fusions contribute to the development of acute leukemia through direct activation of a small set of target genes. We explored an inducible MLL-ENL cellular model, which was obtained from Dr. Robert Slany (University Erlangen, Germany). We wished to examine the differential expressed genes that are bound by MLL wild type (No 4-OHT) and fusion (4-OHT) proteins, combinding the ChIP-chip data to explore the potential MLL fusion-regulated genes.

2011-04-28 | E-GEOD-24794 | biostudies-arrayexpress

hPTTG1-/- HCT116 human colorectal cancer cells: pcDNA3.1 control vs. pcDNA3.1-hPTTG1

Project description:Transcriptional profiling of hPTTG1-/- HCT116 human colorectal cancer cells comparing hPTTG1-/- HCT116 cells transfected with pcDNA3.1, and with hPTTG1-/- HCT116 cells transfected with pcDNA3.1-hPTTG1 plasmid. Two-condition experiment, pchyg vs. 7-2 and 18-2 cells. 1 control, 2 different transfected cells.

2014-01-02 | E-GEOD-26434 | biostudies-arrayexpress

Gene expression regulated by HBV mRNAs

Project description:HBV mRNAs harboring miR-122 response elements were found to bind and sequester endogenous miR-122. This microarray experiment was carried out to find out differentially expressed genes in Huh7 cells expressing HBV mRNAs. RNA was extracted from Huh7 cells transfected with pcDNA3.1 plasmid containing HBV mRNA with wild type (WT) or mutant (Mut) miR-122 response elements in its 3M-bM-^@M-^Y-UTR or the empty pcDNA3.1 vector (3.1) as a mock. Total RNA was then extracted and processed on Affymetrix microarrays in biological duplicate.

2014-12-12 | E-GEOD-64084 | biostudies-arrayexpress

Transcription profiling by array of human control or Wnt11-transfected NTERA-2 cells cultured with DMSO or retinoic acid

Project description:Control or Wnt11-transfected NTERA-2 cells were cultured in the presence of DMSO (control) or 10 micromolar retinoic acid for 5 days

2011-04-10 | E-MEXP-2674 | biostudies-arrayexpress

miRNAs were significantly regulated by myocardin and ERM-NM-1

Project description:Using microarray, we compared miRNAs expression profiles of MDA-MB-231 cells transfected with myocardin and empty vector (pcDNA3.1) and found that 25 miRNAs were significantly changed in myocardin-transfected groups (17 up-regulated and 9 down-regulated miRNAs). Moreover, we showed that 18 of 25 miRNAs significantly regulated by myocardin were inhibited by ERM-NM-1 in MDA-MB-231 cells. In addition,through a microarray approach, we identify the subset of miRNAs modulated by ERM-NM-1 in MDA-MB-231 cells. Our results determined that ERM-NM-1 may function as tumor-promoter through down-regulating expression of 3 miRNAs (miR-26b, miR-146a and miR-331-3p) in MDA-MB-231 cells. There are 4 samples in this experiment (pcDNA3.1-transfected, myocardin-transfected, ERM-NM-1-transfected, myocardin plus ERM-NM-1 co-transfecteded groups) and each sample was replicated 3 times. The vector-pcDNA3.1 was used as control.

2014-10-01 | E-GEOD-44139 | biostudies-arrayexpress

The downstream gene expression of AnxA4 in AGS cells

Project description:AnxA4 expression is increased in H. pylori associated tumors. Moreover, in renal-cell cancer, AnxA4 increases tumor cell dissemination and promotes cell migration, and in colorectal cancer, it is identified as a potential diagnostic marker. How AnxA4 might be involved in tumorgenesis has remained unclear. Here, we compared the gene expression profiles between the cells transfected with pcDNA3.1 (+)/AnxA4 and control (empty vector) to study the downstream genes of AnxA4 using Exon array technique. Four samples are analyzed.

2012-12-20 | E-GEOD-33620 | biostudies-arrayexpress

The truncated somatostatin receptor sst5TMD4 stimulates the angiogenic process and is associated with lymphatic metastasis and poor prognosis in breast cancer patients

Project description:The presence of the truncated somatostatin receptor sst5TMD4 is associated with poor prognosis in breast cancers and increases malignancy in breast cancer cell lines. The objective of this study was to examine the cellular and molecular mechanisms underlying this association in order to identify new molecular targets for diagnosis, prognosis or therapy of these tumors. Therefore, a gene expression array was implemented using sst5TMD4 stably-transfected MCF-7 cells and their respective controls (empty plasmid); which revealed the existence of a profound alteration in the expression of genes involved in several tumoral processes such as cell survival or angiogenesis. Further characterization of sst5TMD4-overexpressing MCF-7 cells demonstrated increased expression/production of key pro-angiogenic factors and enhanced capacity to form mammospheres. These data were confirmed in a xenograft model of in vivo tumoral growth, where inoculation of sst5TMD4 transfected MCF-7 cells induced tumors with higher levels of VEGF and elevated number of blood vessels. Finally, sst5TMD4 was found to be expressed in a subset of human breast cancer samples where it correlated with angiogenic markers (VEGF, Angiopoietin-1 and CD34), the presence of lymphatic metastasis and disease-free survival of the breast cancer patients. Altogether, these data demonstrate a key role of the truncated sst5TMD4 receptor in the control of the angiogenic process during breast cancer progression. Therefore, these results support the role of sst5TMD4 in tumor malignancy and metastatic potential in breast cancers and may help to identifying new lines of actions for future drug therapies for these tumors. Four independent passages from stably-transfected sst5TMD4-pCDNA3.1 and empty-pCDNA3.1 vector, used as control (mock), MFC7 cells were used.

2016-08-04 | E-GEOD-85150 | biostudies-arrayexpress

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