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Metastatic potential in clonal melanomal cells is driven by a rare, early-invading subpopulation [RNA-Seq]

ABSTRACT: To investigate the molecular basis driving a highly invasive phenotype of a rare subpopulation of melanoma cells; The highly invasive phenotype was regulated by the NKX2.2 transcription factor and it was marked by transiently high levels of SEMA3C.

ORGANISM(S): Homo sapiens

PROVIDER: GSE224771 | GEO | 2023/02/13

REPOSITORIES: GEO

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Metastatic potential in clonal melanomal cells is driven by a rare, early-invading subpopulation [ATAC-Seq]

Project description:To investigate the molecular basis driving a highly invasive phenotype of a rare subpopulation of melanoma cells; The highly invasive phenotype was regulated by the NKX2.2 transcription factor and it was marked by transiently high levels of SEMA3C.

2023-02-13 | GSE224769 | GEO

Metastatic potential in clonal melanomal cells is driven by a rare, early-invading subpopulation

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-02-13 | GSE224772 | GEO

An epigenetically distinct breast cancer cell subpopulation promotes collective invasion

Project description:A distinct highly invasive subpopulation was identified in breast cancer cell lines. The molecular characteristics of these cells was investigated, revealing a set of genes whose high expression confers the ability to invade. Total RNA isolated from the invasive subpopulation from 2 cells lines was compared to total RNA isolated from 2 noninvasive populations.

2014-06-19 | E-GEOD-58643 | biostudies-arrayexpress

An epigenetically distinct breast cancer cell subpopulation promotes collective invasion

2014-06-19 | GSE58643 | GEO

Genome-wide analysis of enhancers repressed by Nkx2.2 in spinal motor neuron progenitors

Project description:Unambiguous consolidation of cell identity relies on transcription factors (TFs) acting to suppress alternative lineages, yet few general principles have emerged explaining how repressors manipulate chromatin landscapes to achieve stable gene silencing, especially in instances when these TFs are only temporarily activated. The TF Nkx2.2 is transiently expressed in CNS progenitors yet permanently abrogates somatic motor neuron (sMN) differentiation via interactions with Groucho (Grg) co-repressors. We show that Nkx2.2 inhibits regulatory elements of progenitor and postmitotic sMN transcripts by utilizing Grg to evict co-activators. Surprisingly, co-activator eviction was accomplished using Grg proteins already present at enhancers, rather than through the additional recruitment of Grg or other co-repressors. Nkx2.2-mediated enhancer silencing also led to the loss of H3K27ac modifications from H3K27me3+H3K27ac+ proximal promoters of key sMN genes, facilitating persistent repression of the sMN progenitor program after Nkx2.2 downregulation. These results imply that active loci are poised for suppression, and repressor binding mediates the transition through co-activator displacement.

2023-07-24 | GSE155229 | GEO

Bcl11a (Ctip1) controls migration of cortical projection neurons through regulation of Sema3c

Project description:During neocortical development, neurons undergo polarization, oriented migration, and layer type-specific differentiation. The transcriptional programs underlying these processes are not completely understood. Here we show that the transcription factor Bcl11a regulates polarity and migration of upper layer neurons. Bcl11a-deficient late-born neurons fail to correctly switch from multipolar to bipolar morphology resulting in impaired radial migration. We show that the expression of Sema3c is increased in migrating Bcl11a-deficient neurons and that Bcl11a is a direct negative regulator of Sema3c transcription. In vivo gain-of-function and rescue experiments demonstrate that Sema3c is a major downstream effector of Bcl11a required for the cell polarity switch and for the migration of upper layer neurons. Our data uncover a novel Bcl11a/Sema3c-dependent regulatory pathway used by migrating cortical neurons.

2015-06-17 | GSE52827 | GEO

Genome-wide disclosure of the Nkx2.2 targets in oligodendrocytes and their progenitor cells suggests several novel target genes

Project description:The Nkx2.2 transcription factor contributes to regulate the timing of myelination in the CNS. Still, information about the regulon of Nkx2.2 in oligodendrocytes (Ols) and their progenitor cells (OPCs) is restricted to a few genes. Therefore we aimed to identify the entire regulon of Nkx2.2. We performed transcript profiling of postnatal Nkx2.2-/- mice, investigated the expression of selected transcripts in Ol lineage cells after siRNA induced Nkx2.2 knock-down, and identified the genome-wide active Nkx2.2 binding sites in murine OPCs and Ols by use of ChIP-sequencing technique. Thereby we have found 521 genes with active Nkx2.2 binding sites within 10,000 bp of their gene loci that furthermore are differently expressed in absence or lower expression of Nkx2.2. Functionally, the target genes are associated with mitosis, migration stop, protein transport, lipid metabolism, mitochondrial biogenesis, formation of Ca2+ waves, and WNT signalling. Furthermore, motif discovery techniques and tests for overlaps between sequencing reads suggest that MYRF, OLIG2, SOX10, and TCF3 interact or compete with Nkx2.2 in OPCs/Ols. However, the activator versus repressor activity of Nkx2.2 does not seem to depend on the potential interaction with either of the transcription factors. Test for overlaps with sites of specific histone 3 modifications show that the Nkx2.2 binding sites are more frequently associated H3K4me3 and H3K27ac in genes to which Nkx2.2 may act as an activator. This supports previous studies showing that Nkx2.2 acts in a HDAC1 dependent way. Together this provides new insight into how Nkx2.2 contributes to the timing of OPC differentiation and myelination in CNS.

2019-11-01 | GSE73921 | GEO

Genome-wide disclosure of the Nkx2.2 targets in oligodendrocytes and their progenitor cells suggests several novel target genes

2020-09-30 | GSE73664 | GEO

NKX2.2

Project description:NKX2.2

| PRJNA316849 | ENA

Global profiling of Nkx2.2 SD-domain mutant pancreas during development and adulthood compared to transcriptional profiling of SD-domain mutant expressing neural progenitors.

Project description:The consolidation of unambiguous cell fate commitment relies on the ability of transcription factors (TFs) to exert tissue-specific regulation of complex genetic networks. The mechanisms by which TFs establish such precise control over gene expression, however, have remained elusive—especially in instances where a single TF operates in two or more discrete cellular systems. In this study, we demonstrate that  cell specific functions of NKX2.2 are driven by the highly conserved NK2-Specific Domain (SD). Mutation of the endogenous NKX2.2 SD domain prevents the developmental progression of beta cell precursors into mature, insulin-expressing beta cells, resulting in overt neonatal diabetes. Within the adult beta cell, the SD domain stimulates beta cell performance through the activation and repression of a subset of NKX2.2-regulated transcripts critical for beta cell function. These irregularities in beta cell gene expression may be mediated via SD domain-contingent interactions with components of the nuclear pore complex. In stark contrast to these pancreatic phenotypes, however, the SD domain is entirely dispensable for the development of NKX2.2-dependent cell types within the CNS. Together, these results reveal a previously undetermined mechanism through which NKX2.2 directs disparate transcriptional programs in the pancreas vs. neuroepithelium.

2024-02-21 | GSE226345 | GEO

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