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Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation [scRNA-Seq]

ABSTRACT: Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation [scRNA-Seq]

PROVIDER: PRJNA992517 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25195118.fastq.gz	Fastqsanger.gz
	SRR25195119_1.fastq.gz	Fastqsanger.gz
	SRR25195119_2.fastq.gz	Fastqsanger.gz
	SRR25195120_1.fastq.gz	Fastqsanger.gz
	SRR25195120_2.fastq.gz	Fastqsanger.gz

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Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation

Project description:Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation

| PRJNA992513 | ENA

Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation [RNA-Seq]

Project description:Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation [RNA-Seq]

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Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation [ATAC-Seq]

Project description:Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation [ATAC-Seq]

| PRJNA992520 | ENA

Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation [ATAC-Seq]

Project description:The early mechanisms of spontaneous tumor initiation that precede the accumulation of cancer mutations are largely unknown. We show that reduced aPKC levels correlate with stem cell loss and the induction of revival and metaplastic programs in serrated- and conventional-initiated pre-neoplastic lesions, which is perpetuated in colorectal cancers (CRC). Acute inactivation of PKCl/i in vivo and in organoids is sufficient to stimulate JNK in non-transformed intestinal epithelial cells (IECs), which promotes cell death and the rapid loss of the intestinal stem cells (ISC), including LGR5+ cells. This is followed by the accumulation of revival stem cells (RSC) at the bottom of the crypt and fetal metaplastic cells (FMC) at the top, creating two spatiotemporally distinct cell populations that depend on JNK-induced AP-1 and YAP. These cell lineage changes are maintained during cancer initiation and progression and determine the aggressive phenotype of human CRC irrespective of their serrated or conventional origin

2023-11-07 | GSE236850 | GEO

Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation [scRNA-Seq]

2023-11-07 | GSE236848 | GEO

Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation [RNA-Seq]

2024-07-05 | GSE236649 | GEO

Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation.

Project description: Not available

| S-EPMC11303105 | biostudies-literature

Epithelial aPKC deficiency leads to stem cell loss preceding metaplasia in colorectal cancer initiation

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

2023-11-07 | GSE236851 | GEO

Expression data from TGFbeta-treated control or aPKC silenced A549 cells

Project description:Aberrant TGFbeta signalling is a hallmark of epithelial derived tumours. Signalling patterns can depend on the membrane trafficking and internalization of the TGFbeta receptors. Protein kinase C (PKC), particularly the atypical PKC isoforms, alter the trafficking of TGFbeta receptors and can alter TGFbeta induced gene expression. We used microarrays to detail the programme of gene expression underlying TGFbeta induction between control or aPKC silenced A549 cells. Control or aPKC silenced A549 cells were serum starved and treated with TGFbeta for 1 hour. Total RNA was extracted from untreated or TGFbeta treated cells after 8 and 24 hours and analyzed using Affymetrix microarrays. We sought to assess TGFbeta gene expression in aPKC silenced lung cancer cells, as we found that knockdown of aPKC extends TGFbeta signalling as assessed by phospho Smad2 levels. Furthermore, increased expression and oncogenic activity of aPKC (PKCiota) has been reported in lung cancer cells.

2011-01-29 | E-GEOD-26241 | biostudies-arrayexpress

aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA binding ability

Project description:Strict regulation of proliferation is vital for development, whereas unregulated cell proliferation is a fundamental characteristic of cancer. The polarity protein atypical protein kinase C lambda/iota (aPKC lambda) is associated with cell proliferation through unknown mechanisms. In endothelial cells, suppression of aPKC lambda impairs proliferation despite hyperactivated mitogenic signaling. Here we show that aPKC lambda phosphorylates the DNA binding domain of forkhead box O1 (FoxO1) transcription factor, a gatekeeper of endothelial growth. Although mitogenic signaling excludes FoxO1 from the nucleus, consequently increasing c-Myc abundance and proliferation, aPKC lambda controls c-Myc expression via FoxO1/miR-34c signaling without affecting its localization. We find this pathway is strongly activated in the malignant vascular sarcoma, angiosarcoma, and aPKC inhibition reduces c-Myc expression and proliferation of angiosarcoma cells. Moreover, FoxO1 phosphorylation at Ser218 and aPKC expression correlates with poor patient prognosis. Our findings may provide a new therapeutic strategy for treatment of malignant cancers, like angiosarcoma.

2019-11-12 | PXD011595 | Pride

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