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Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, SOX2 and CD44 through NFκB signaling

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE264191 | GEO | 2024/08/21

REPOSITORIES: GEO

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Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, SOX2, and CD44 through NFκB-signaling

Project description: Not available

| S-EPMC11340773 | biostudies-literature

Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, SOX2 and CD44 through NFκB signaling [LNCaP]

Project description:The inflammatory tumor microenvironment (TME) is a key driver of tumor-promoting processes. Tumor-associated macrophages are one of the main immune cell types in the TME and their density increases during cancer progression. Here, we investigated the influence of pro-inflammatory (M1) and immunosuppressive (M2) macrophages on prostate cancer lineage plasticity. Our findings reveal that M1 macrophage secreted factors upregulate genes related to stemness while downregulating genes associated with androgen response in LNCaP prostate cancer cells. Cancer stem cell plasticity markers NANOG, KLF4, SOX2, OCT4 and CD44 were stimulated by the secreted factors from M1 macrophages. Moreover, AR and its target gene KLK3 were observed to be suppressed in LNCaP cells treated exposed to secreted factors from M1 macrophages. Inhibition of NF-κB signaling using the IKK16 inhibitor resulted in downregulation of NANOG, SOX2 and CD44. Our study highlights that the secreted factors from M1 macrophages drive prostate cancer cell plasticity by upregulating the expression of cancer stem cell plasticity markers through NF-κB signaling pathway.

2024-08-21 | GSE251851 | GEO

Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, SOX2 and CD44 through NFκB signaling [LNCaP-C42B]

Project description:The inflammatory tumor microenvironment (TME) is a key driver of tumor-promoting pro-cesses. Tumor-associated macrophages are one of the main immune cell types in the TME and their increased density is related to poor prognosis in prostate cancer. Here, we investigated the influence of pro-inflammatory (M1) and immunosuppressive (M2) macrophages on pros-tate cancer lineage plasticity. Our findings reveal that M1 macrophage secreted factors up-regulate genes related to stemness while downregulating genes associated with androgen re-sponse in prostate cancer cells. The expression of cancer stem cell plasticity markers NANOG, KLF4, SOX2, OCT4 and CD44 was stimulated by the secreted factors from M1 macrophages. Moreover, AR and its target gene KLK3 were observed to be suppressed in LNCaP cells treated with secreted factors from M1 macrophages. Inhibition of NFκB signaling using the IKK16 inhibitor resulted in downregulation of NANOG, SOX2 and CD44 and cancer stem cell plasticity. Our study highlights that the secreted factors from M1 macrophages drive prostate cancer cell plasticity by upregulating the expression of cancer stem cell plasticity markers through NFκB signaling pathway.

2024-08-21 | GSE264190 | GEO

Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, SOX2 and CD44 through NFκB signaling

Project description:Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, SOX2 and CD44 through NFκB signaling

| PRJNA1101426 | ENA

Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, SOX2 and CD44 through NFκB signaling [LNCaP]

Project description:Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, SOX2 and CD44 through NFκB signaling [LNCaP]

| PRJNA1055556 | ENA

Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, SOX2 and CD44 through NFκB signaling [LNCaP-C42B]

Project description:Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG, SOX2 and CD44 through NFκB signaling [LNCaP-C42B]

| PRJNA1101428 | ENA

SUMOylation represses Nanog expression via modulating transcription factors Oct4 and Sox2.

Project description:Nanog is a pivotal transcription factor in embryonic stem (ES) cells and is essential for maintaining the pluripotency and self-renewal of ES cells. SUMOylation has been proved to regulate several stem cell markers' function, such as Oct4 and Sox2. Nanog is strictly regulated by Oct4/Sox2 heterodimer. However, the direct effects of SUMOylation on Nanog expression remain unclear. In this study, we reported that SUMOylation repressed Nanog expression. Depletion of Sumo1 or its conjugating enzyme Ubc9 increased the expression of Nanog, while high SUMOylation reduced its expression. Interestingly, we found that SUMOylation of Oct4 and Sox2 regulated Nanog in an opposing manner. SUMOylation of Oct4 enhanced Nanog expression, while SUMOylated Sox2 inhibited its expression. Moreover, SUMOylation of Oct4 by Pias2 or Sox2 by Pias3 impaired the interaction between Oct4 and Sox2. Taken together, these results indicate that SUMOylation has a negative effect on Nanog expression and provides new insights into the mechanism of SUMO modification involved in ES cells regulation.

| S-EPMC3382131 | biostudies-literature

SOX2, OCT3/4 and NANOG expression and cellular plasticity in rare human somatic cells requires CD73.

Project description:Endogenous Plastic Somatic (ePS) cells isolated from adult human tissues exhibit extensive lineage plasticity in vitro and in vivo. Here we visualize these rare ePS cells in a latent state, i.e. lacking SOX2, OCT3/4 and NANOG (SON) expression, in non-diseased breast specimens through immunohistochemical analysis of previously identified ePS-specific biomarkers (CD73+, EpCAM+ and CD90-). We also report a novel mechanism by which these latent ePS cells acquire SON expression and plasticity in vitro. Four extracellular factors are necessary for the acquisition of SON expression and lineage plasticity in ePS cells: adenosine (which is produced by the 5' ecto-nucleotidase CD73 and activates in turn the PKA-dependent IL6/STAT3 pathway through the adenosine receptor ADORA2b), IL6, FGF2 and ACTIVIN A. Blocking any pathway component renders ePS cells incapable of SON expression and lineage plasticity. Notably, hESCs do not use adenosine or IL6 nor they express CD73 or ADORA2b and inhibition of adenosine signaling does not ablate their plasticity. Therefore, the data presented here delineate novel circuitry and physiological signals for accessing SON expression in rare, undifferentiated human cells.

| S-EPMC5107210 | biostudies-literature

OCT4/SOX2-independent Nanog autorepression modulates heterogeneous Nanog gene expression in mouse ES cells.

Project description:NANOG, OCT4 and SOX2 form the core network of transcription factors supporting embryonic stem (ES) cell self-renewal. While OCT4 and SOX2 expression is relatively uniform, ES cells fluctuate between states of high NANOG expression possessing high self-renewal efficiency, and low NANOG expression exhibiting increased differentiation propensity. NANOG, OCT4 and SOX2 are currently considered to activate transcription of each of the three genes, an architecture that cannot readily account for NANOG heterogeneity. Here, we examine the architecture of the Nanog-centred network using inducible NANOG gain- and loss-of-function approaches. Rather than activating itself, Nanog activity is autorepressive and OCT4/SOX2-independent. Moreover, the influence of Nanog on Oct4 and Sox2 expression is minimal. Using Nanog:GFP reporters, we show that Nanog autorepression is a major regulator of Nanog transcription switching. We conclude that the architecture of the pluripotency gene regulatory network encodes the capacity to generate reversible states of Nanog transcription via a Nanog-centred autorepressive loop. Therefore, cellular variability in self-renewal efficiency is an emergent property of the pluripotency gene regulatory network.

| S-EPMC3545296 | biostudies-literature

Structural mechanism of DNA-mediated Nanog-Sox2 cooperative interaction.

Project description:The efficiency of stem cell transcriptional regulation always depends on the cooperative association and expression of transcription factors (TFs). Among these, Oct4, Sox2, and Nanog play major roles. Their cooperativity is facilitated via direct protein-protein interactions or DNA-mediated interactions, yet the mechanism is not clear. Most biochemical studies have examined Oct4/Sox2 cooperativity, whereas few studies have evaluated how Nanog competes in the connection between these TFs. In this study, using computational models and molecular dynamics simulations, we built a framework representing the DNA-mediated cooperative interaction between Nanog and Sox2 and analyzed the plausible interaction factors experienced by Nanog because of Sox2, its cooperative binding partner. Comparison of a wild-type and mutant Nanog/Sox2 model with the Nanog crystal structure revealed the regulatory structural mechanism between Nanog/Sox2-DNA-mediated cooperative bindings. Along with the transactivation domains interaction, the DNA-mediated allosteric interactions are also necessary for Nanog cooperative binding. DNA-mediated Nanog-Sox2 cooperativity influences the protein conformational changes and a stronger interaction profile was observed for Nanog-Mut (L103E) in comparison with the Nanog-WT complex.

| S-EPMC9061787 | biostudies-literature

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