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

PROVIDER: PRJNA1101426 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27319700_1.fastq.gz	Fastqsanger.gz
	SRR27319700_2.fastq.gz	Fastqsanger.gz
	SRR27319701_1.fastq.gz	Fastqsanger.gz
	SRR27319701_2.fastq.gz	Fastqsanger.gz
	SRR27319702_1.fastq.gz	Fastqsanger.gz

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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 [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]

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

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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]

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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

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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:This SuperSeries is composed of the SubSeries listed below.

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NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells

Project description:This SuperSeries is composed of the following subset Series: GSE34904: NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 1) GSE34912: NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 2) GSE34918: NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 3) GSE34920: NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 4) Refer to individual Series

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NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 4)

Project description:The transcription factors Nanog, Oct4 and Sox2 are the master regulators of pluripotency in mouse embryonic stem cells (mESCs), however, their functions in human ESCs (hESCs) have not been rigorously defined. Here we show that the requirements for NANOG, OCT4 and SOX2 in hESCs differ from those in mESCs. Both NANOG and OCT4 are required for self-renewal and repress differentiation. OCT4 controls both extraembryonic and epiblast-derived cell fates in a BMP4-dependent manner. OCT4-depleted hESCs commit to trophectoderm and primitive endoderm in the presence of BMP4, but undergo neuroectoderm differentiation in the absence of BMP4. NANOG represses neuroectoderm and neural crest commitment, but has little or no effect on the other lineages. We find that SOX2 is not required for self-renewal because it is redundant with SOX3, which is induced in SOX2-depleted hESCs. Simultaneous depletion of both SOX2 and SOX3 induces differentiation into the primitive streak. Unexpectedly, we identify significant variability in the usage of pluripotency factors by individual hESC lines, suggesting that the pluripotency network is remodelled to support a continuum of developmental states. Our study revises the general view of how NANOG, OCT4 and SOX2 orchestrate self-renewal in hESCs.

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NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 3)

2012-04-06 | GSE34918 | GEO

NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 2)

2012-04-06 | GSE34912 | GEO