RNA-seq of CLB-GA neuroblastoma cell line upon TBX2 knockdown
Ontology highlight
ABSTRACT: RNA-seq upon TBX2 knockdown in the neuroblastoma cell line CLB-GA. Cells were transduced with two different shRNAs (sh#2 and sh#4) targeting TBX2 and a non-targeting control (NTC), and selected with puromycin. Analysis was performed seven days upon TBX2 knockdown, including three biological replicates per condition.
Project description:RNA-seq upon TBX2, MYCN or combination of TBX2 and MYCN knockdown in the neuroblastoma cell line IMR-5/75. Cells were transduced with two different shRNAs (shTBX2_2 and shTBX2_4) targeting TBX2 and a non-targeting control (NTC), and selected with puromycin. Cells were treated with doxycycline for shMYCN induction (with DOX or not). Analysis was performed three days upon TBX2 knockdown and two days upon MYCN knockdown, including six biological replicates per condition.
Project description:RNA-seq to define downstream targets of adrenergic SOX11 upon 1ug/ml doxycyline inducible SOX11 overexpression in a SOX11 non-expressing mesenchymal cell line SH-EP. Analysis was performed 48h upon treatment with doxycycline, control samples are the untreated cells. 3 biological replicates from different monoclonal expansions (F2, C11, G2) of SH-EP cells were used.
Project description:RNA-seq to define downstream targets of adrenergic SOX11 upon 1ug/ml doxycyline inducible SOX11 overexpression in a SOX11 non-expressing mesenchymal cell line SH-EP. Analysis was performed 48h upon treatment with doxycycline, control samples are the untreated cells. 2 biological replicates were used.
Project description:ChIP-seq to define bindings sites for TBX2, MYCN, H3K27ac, H3K4me1, H3K4me3 and Input in the cell lines IMR-32, CLB-GA, NGP, IMR-5/75, GI-M-EN, CHP-212, and IMR-5.
Project description:RNA-seq to define downstream targets of adrenergic SOX11 upon knockdown using 4 siRNAs against SOX11 in the SOX11 expressing adrenergic cell line IMR-32. Analysis was performed 48h upon after nucleofections, control samples are treated with siNTC (non-targeted control). 4 biological replicates were used.
Project description:We report the high-throughput profiling of Tbx2 binding sites in mouse melanoma B16 cells. We generated B16 clones that have endogenous Tbx2 tagged with 3xHA, and used HA antibody for immunoprecipitation. This study provides a high-quality genome-wide Tbx2 binding profile and helps further understand Tbx2 role in melanoma progression
Project description:Here we demonstrate a previously unknown mechanism of TBX2-mediated gene repression in breast tumours, whereby TBX2 physically interacts with CoREST-associated proteins LSD1, HDAC1 and the ZNF217 oncogene. Through Chromatin Immunoprecipitation sequencing (ChIP-seq) we find that while over 80% of TBX2 binding sites are concentrated at promoters, these regions show remarkably no enrichment for the T-box element; rather TBX2-bound regions are biased toward a small number of non-T-box motifs, with the most abundant being Specificity Protein 1 (Sp1), EGR1 and Nuclear Transcription Factor Y (NF-Y). Furthermore, we uncover that Sp1 is crucial for recruitment of TBX2 to the NDRG1 promoter and subsequent repression of this gene. We also observe that ZNF217 cooccupies approximately 30% of TBX2-bound sites, a number of which contain RCOR1 and exhibit upregulation of the associated transcripts following disruption of TBX2/CoREST function. Overall these data highlight a novel potential therapeutic opportunity whereby poor-prognosis, TBX2 overexpressing breast tumours may be pharmacologically exploited by targeting the CoREST-dependent gene repression network, to recover normal growth control.
Project description:Atoh1 is essential for the development of both outer hair cells (OHCs) and inner hair cells (IHCs) in the mammalian cochlea. Whereas Ikzf2 is necessary for OHC development, the key gene required for IHC development remains unknown. We found that deletion of Tbx2 in neonatal IHCs led to their transdifferentiation into OHCs by repressing 26.7% of IHC genes and inducing 56.3% of OHC genes, including Ikzf2. More importantly, persistent expression of Tbx2 coupled with transient Atoh1 expression effectively reprogramed non-sensory supporting cells into new IHCs expressing the functional IHC marker vGlut3. The differentiation status of these new IHCs was considerably more advanced than that previously reported. Thus, Tbx2 is essential for IHC development, and co-upregulation of Tbx2 with Atoh1 in supporting cells represents a new approach for treating deafness related to IHC degeneration.