Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Growth arrest of human thyroid cancer cells 8505C after inhibition of TTF-1 transcriptional activity

ABSTRACT: Background: thyroid transcription factor-1 (TTF-1) is known to play key roles in thyroid organogenesis, in thyroid cell proliferation and in the expression of genes involved in thyroid differentiated function. Objective: to understand why many human thyroid cancer cell lines keep producing TTF-1 despite the loss of differentiation. Methods: a chimeric protein acting as a functional antagonist of TTF-1 transcriptional activity was expressed conditionally in 8505C cells originating from an undifferentiated thyroid carcinoma. The consequences of the inhibition of TTF-1 activity in the cells expressing the antagonist on cell proliferation, mRNA and miRNA expression were analyzed. Results: we observed a growth arrest of 8505C thyroid cancer cells when the endogenous TTF-1 transcriptional activity was inhibited. It correlated with decreased levels of several mRNAs encoding positive effectors of cell proliferation like CDK1 and cyclinB1, and increased levels of various mRNAs encoding negative regulators of cell division like CDKN2B and DUSP6. By contrast, no significant change was observed in the miRNA population. Conclusion: the persistence of TTF-1 expression observed in most dedifferentiated human thyroid cancer cell lines is likely to be explained by the fact that TTF-1 activity is still required for proliferation of these tumor cells as demonstrated here in the 8505C cell line.

ORGANISM(S): Homo sapiens

PROVIDER: GSE58243 | GEO | 2016/06/01

SECONDARY ACCESSION(S): PRJNA251721

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Growth arrest of human thyroid cancer cells 8505C after inhibition of TTF-1 transcriptional activity

Project description:Background: thyroid transcription factor-1 (TTF-1) is known to play key roles in thyroid organogenesis, in thyroid cell proliferation and in the expression of genes involved in thyroid differentiated function. Objective: to understand why many human thyroid cancer cell lines keep producing TTF-1 despite the loss of differentiation. Methods: a chimeric protein acting as a functional antagonist of TTF-1 transcriptional activity was expressed conditionally in 8505C cells originating from an undifferentiated thyroid carcinoma. The consequences of the inhibition of TTF-1 activity in the cells expressing the antagonist on cell proliferation, mRNA and miRNA expression were analyzed. Results: we observed a growth arrest of 8505C thyroid cancer cells when the endogenous TTF-1 transcriptional activity was inhibited. It correlated with decreased levels of several mRNAs encoding positive effectors of cell proliferation like CDK1 and cyclinB1, and increased levels of various mRNAs encoding negative regulators of cell division like CDKN2B and DUSP6. By contrast, no significant change was observed in the miRNA population. Conclusion: the persistence of TTF-1 expression observed in most dedifferentiated human thyroid cancer cell lines is likely to be explained by the fact that TTF-1 activity is still required for proliferation of these tumor cells as demonstrated here in the 8505C cell line. Microarrays miRNA hybridizations were performed on 8505c cells expressing a TTF1 antagonist (Engr HD âDox) versus non-expressing cells (Engr HD +Dox), on cells expressing the control protein (Engr HDm â Dox) versus non-expressing cells (Engr HDm + Dox), and on cell expressing the TTF1 antagonist (Engr HDâ Dox) versus the cells expressing the control protein (Engr HDmâ Dox). Hybridizations were replicated with dye swap.

2016-06-01 | E-GEOD-58243 | biostudies-arrayexpress

Growth arrest of human thyroid cancer cells 8505C after inhibition of TTF-1 transcriptional activity

Project description:Background: thyroid transcription factor-1 (TTF-1) is known to play key roles in thyroid organogenesis, in thyroid cell proliferation and in the expression of genes involved in thyroid differentiated function. Objective: to understand why many human thyroid cancer cell lines keep producing TTF-1 despite the loss of differentiation. Methods: a chimeric protein acting as a functional antagonist of TTF-1 transcriptional activity was expressed conditionally in 8505C cells originating from an undifferentiated thyroid carcinoma. The consequences of the inhibition of TTF-1 activity in the cells expressing the antagonist on cell proliferation, mRNA and miRNA expression were analyzed. Results: we observed a growth arrest of 8505C thyroid cancer cells when the endogenous TTF-1 transcriptional activity was inhibited. It correlated with decreased levels of several mRNAs encoding positive effectors of cell proliferation like CDK1 and cyclinB1, and increased levels of various mRNAs encoding negative regulators of cell division like CDKN2B and DUSP6. By contrast, no significant change was observed in the miRNA population. Conclusion: the persistence of TTF-1 expression observed in most dedifferentiated human thyroid cancer cell lines is likely to be explained by the fact that TTF-1 activity is still required for proliferation of these tumor cells as demonstrated here in the 8505C cell line. Microarrays hybridizations were performed on human thyroid cancer cells 8505C expressing a TTF1 antagonist (Engr HD –Dox) versus non-expressing cells (Engr HD +Dox) and versus cells expressing the control protein (Engr HDm – Dox). After amplification and labelling, sample pairs were hybridized onto HS1100_Human_MI_ReadyArray (Microarrays Inc., Huntsville, AL, USA). The oligonucleotide set consists of 40,604 70-mer probes that were designed using a transcriptome-based annotation of exonic structure for genomic loci. Hybridizations were replicated with dye swap.

2015-06-15 | E-GEOD-58587 | biostudies-arrayexpress

Growth arrest of human thyroid cancer cells 8505C after inhibition of TTF-1 transcriptional activity

2015-06-15 | GSE58587 | GEO

RNA-seq of anaplastic thyroid carcinoma cell line (8505c) after overexpression of OVOL2

Project description:Identification of OVOL2-related transcriptional program in anaplastic thyroid carcinoma-derived cell line, 8505c. Doxycycline-inducible system was obtained by infecting 8505c cells with lentiviral vector containing OVOL2 coding sequence fused with HA tag. Control cells were infected with empty vector (EV). Cells were collected 24 hours upon doxycycline treatment.

2023-10-05 | E-MTAB-11055 | biostudies-arrayexpress

Functional inactivation of Thyroid Transcription Factor-1 in PCCl3 thyroid cells

Project description:Thyroid Transcription Factor-1 (TTF-1) is a key regulator of thyroid development and function. In order to identify the genes whose expression depends on TTF-1 transcriptional activity within the thyrocyte we analyzed the consequence of the functional inactivation of this factor in PCCl3 cells. The expression of a fusion protein composed of the DNA binding domain of TTF-1 and of the strong repressive domain of the Engrailed protein (Engr HD) resulted in a dramatic loss of epithelial cell morphology and in proliferation arrest. These changes were reversed when the inhibition of endogenous TTF-1 was relieved. No change was observed when a similar fusion protein containing point mutations abolishing DNA binding activity (Engr HDm) was produced in the cells.

2012-07-01 | GSE35623 | GEO

Validation of the Personalized Gene Therapy by stably transfection of PANK2 in the papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines

Project description:An ideal cancer gene therapy would selectively destroy the cancer cells without affecting much the healthy tissue. This would be possible if and only if the cancer and normal cells of the tumor are governed by distinct gene master regulators (GMRs). Logic dictates that, while being strongly protected by the homeostatic mechanisms, expression of a GMR governs the phenotype by modulating major functional pathways through controlling the expression of the involved genes. We determined the GMRs of the standard papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. The hierarchy of the known biomarkers was established based on their gene commanding height (GCH), an original measure combining the expression control and coordination with expression of other genes. We found that the sets of the GMRs are largely different in the two thyroid cancer cell lines, indicatibg that each type of thyroid cancer needs a different gene-targeting therapy. In this experiment, we determined the transcriptomic effects of the stable transfection of PANK2 gene In the papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. PANK2 was selected because it has significantly different GCHs in the two cell lines: 44.64 in BCPAP and 3.61 in 8505C. The significantly more up- and down-regulated genes in the transfected BCPAP than in the transfected 8505C cells compared to their untransfected counterparts validated the theory and indicated the usefulness of our personalized gene therapy approach.

2017-03-25 | GSE97030 | GEO

Validation of the Personalized Gene Therapy by stably transfection of UBALD1 in the papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines

Project description:An ideal cancer gene therapy would selectively destroy the cancer cells without affecting much the healthy tissue. This would be possible if and only if the cancer and normal cells of the tumor are governed by distinct gene master regulators (GMRs). Logic dictates that, while being strongly protected by the homeostatic mechanisms, expression of a GMR governs the phenotype by modulating major functional pathways through controlling the expression of the involved genes. We determined the GMRs of the standard papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. The hierarchy of the known biomarkers was established based on their gene commanding height (GCH), an original measure combining the expression control and coordination with expression of other genes. We found that the sets of the GMRs are largely different in the two thyroid cancer cell lines, indicatibg that each type of thyroid cancer needs a different gene-targeting therapy. In this experiment, we determined the transcriptomic effects of the stable transfection of UBALD1 gene in the BCPAP and 8505C thyroid cancer cell lines. UBALD1 was selected because it has significantly different GCHs in the two cell lines: 10.31 in 8505C and 1.12 in BCPAP. The significantly more up- and down-regulated genes in the transfected 8505C cells than in the transfected BCPAP cells compared to their untransfected counterparts validated the theory and indicated the usefulness of our personalized gene therapy approach.

2017-04-06 | GSE97427 | GEO

Validation of the Personalized Gene Therapy by stably transfection of DDX19B in the papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines

Project description:An ideal cancer gene therapy would selectively destroy the cancer cells without affecting much the healthy tissue. This would be possible if and only if the cancer and normal cells of the tumor are governed by distinct gene master regulators (GMRs). Logic dictates that, while being strongly protected by the homeostatic mechanisms, expression of a GMR governs the phenotype by modulating major functional pathways through controlling the expression of the involved genes. We determined the GMRs of the standard papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. The hierarchy of the known biomarkers was established based on their gene commanding height (GCH), an original measure combining the expression control and coordination with expression of other genes. We found that the sets of the GMRs are largely different in the two thyroid cancer cell lines, indicatibg that each type of thyroid cancer needs a different gene-targeting therapy. In this experiment, we determined the transcriptomic effects of the stable transfection of DDX19B gene In the papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. DDX19B was selected because it has significantly different GCHs in the two cell lines: 1.64 in BCPAP and 6.03 in 8505C. The significantly more up- and down-regulated genes in the transfected 8505C than in the transfected BCPAP cells compared to their untransfected counterparts validated the theory and indicated the usefulness of our personalized gene therapy approach.

2017-03-25 | GSE97028 | GEO

Validation of the Personalized Gene Therapy by stably transfection of NEMP1 (TMEM194A) in the papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines

Project description:An ideal cancer gene therapy would selectively destroy the cancer cells without affecting much the healthy tissue. This would be possible if and only if the cancer and normal cells of the tumor are governed by distinct gene master regulators (GMRs). Logic dictates that, while being strongly protected by the homeostatic mechanisms, expression of a GMR governs the phenotype by modulating major functional pathways through controlling the expression of the involved genes. We determined the GMRs of the standard papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. The hierarchy of the known biomarkers was established based on their gene commanding height (GCH), an original measure combining the expression control and coordination with expression of other genes. We found that the sets of the GMRs are largely different in the two thyroid cancer cell lines, indicatibg that each type of thyroid cancer needs a different gene-targeting therapy. In this experiment, we determined the transcriptomic effects of the stable transfection of NEMP1 (TMEM194A) gene encoding a nuclear envelope protein in the papillary (BCPAP) and anaplastic (8505C) thyroid cancer cell lines. NEMP1 was selected because it has significantly different GCHs in the two cell lines: 5.95 in BCPAP and 0.40 in 8505C. The significantly more up- and down-regulated genes in the transfected BCPAP than in the transfected 8505C cells compared to their untransfected counterparts validated the theory and indicated the usefulness of our personalized gene therapy approach.

2017-03-25 | GSE97031 | GEO

RNA-seq of anaplastic thyroid carcinoma cells (CAL62 and 8505c) after E2F7 silencing

Project description:Gene expression comparison between anaplastic thyroid carcinoma cells (CAL62 and 8505c) transfected with si-RNA against E2F7 or scramble oligos, with the intent of defining the gene expression program under the control of this transcription factor in this tumor subtype.

2023-02-07 | E-MTAB-9788 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data