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Metastatic potential in clonal melanomal cells is driven by a rare, early-invading subpopulation [ATAC-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: GSE224769 | GEO | 2023/02/13

REPOSITORIES: GEO

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Metastatic potential in clonal melanomal cells is driven by a rare, early-invading subpopulation [RNA-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 | GSE224771 | 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

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

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

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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

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

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

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

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

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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

Semaphorin 3C (Sema3C) reshapes stromal microenvironment to promote hepatocellular carcinoma progression

Project description:More than 90% of hepatocellular carcinoma (HCC) cases develop in the presence of fibrosis or cirrhosis, making the tumor microenvironment (TME) of HCC distinctive due to the intricate interplay between cancer-associated fibroblasts (CAFs) and cancer stem cells (CSCs), which collectively regulate HCC progression. However, the mechanisms through which CSCs orchestrate the dynamics of the tumor stroma during HCC development remain elusive. Our study unveils a significant upregulation of Sema3C in fibrotic liver, HCC tissues, peripheral blood of HCC patients, as well as sorafenib-resistant tissues and cells, with its overexpression correlating with the acquisition of stemness properties in HCC. We further identify NRP1 and ITGB1 as pivotal functional receptors of Sema3C, activating downstream AKT/Gli1/c-Myc signaling pathways to bolster HCC self-renewal and tumor initiation. Additionally, HCC cells-derived Sema3C facilitated extracellular matrix (ECM) contraction and collagen deposition in vivo, while also promoting the proliferation and activation of hepatic stellate cells (HSCs). Mechanistically, Sema3C interacted with NRP1 and ITGB1 in HSCs, activating downstream NF-kB signaling, thereby stimulating the release of IL-6 and upregulating HMGCR expression, consequently enhancing cholesterol synthesis in HSCs. Furthermore, CAF-secreted TGF-β1 activates AP1 signaling to augment Sema3C expression in HCC cells, establishing a positive feedback loop that accelerates HCC progression. Notably, blockade of Sema3C effectively inhibits tumor growth and sensitizes HCC cells to sorafenib in vivo. In sum, our findings spotlight Sema3C as a novel biomarker facilitating the crosstalk between CSCs and stroma during hepatocarcinogenesis, thereby offering a promising avenue for enhancing treatment efficacy and overcoming drug resistance in HCC.

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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

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