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Impaired immunosurveillance by the simultaneous loss of both atypical PKCs drives intestinal cancer through the serrated pathway [IECs DKO aPKC]

ABSTRACT: Impaired immunosurveillance by the simultaneous loss of both atypical PKCs drives intestinal cancer through the serrated pathway [IECs DKO aPKC]

PROVIDER: PRJNA430359 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6496950.fastq.gz	Fastqsanger.gz
	SRR6496960.fastq.gz	Fastqsanger.gz
	SRR6496970.fastq.gz	Fastqsanger.gz
	SRR6496980.fastq.gz	Fastqsanger.gz
	SRR6496990.fastq.gz	Fastqsanger.gz

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Impaired immunosurveillance by the simultaneous loss of both atypical PKCs drives intestinal cancer through the serrated pathway [IECs DKO aPKC]

Project description:The serrated adenocarcinoma subtype accounts for 15-30% of all colorectal cancers (CRCs) and is aggressive and treatment-resistant. it is an alternative mechanism for CRC development characterized by dysregulation of the MAPK pathway. We show that human serrated tumors display reduced expression of PKCz and PKCl/i, and that the simultaneous inactivation of these genes in the mouse intestinal epithelium resulted in spontaneous tumorigenesis through the serrated pathway that progressed to advanced cancer. Whereas epithelial PKCl/i deficiency led to immunogenic cell death that repressed tumor initiation, interferon and CD8+ T cell responses were impaired concomitant with stromal activation and immunosuppression driven by PKCz loss. Thus, PKCz and PKCl/i cooperatively suppress serrated tumorigenesis. Targeting this stromal activation and immunosuppression showed synergistic curative activity.

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Impaired immunosurveillance by the simultaneous loss of both atypical PKCs drives serrated intestinal cancer

Project description:Impaired immunosurveillance by the simultaneous loss of both atypical PKCs drives serrated intestinal cancer

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Impaired immunosurveillance by the simultaneous loss of both atypical PKCs drives serrated intestinal cancer

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Impaired immunosurveillance by the simultaneous loss of both atypical PKCs drives intestinal cancer through the serrated pathway

Project description:Impaired immunosurveillance by the simultaneous loss of both atypical PKCs drives intestinal cancer through the serrated pathway

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

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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.

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Project description:Serrated adenocarcinomas are morphologically different from conventional adenocarcinomas. The serrated pathway has recently been proposed to represent a novel mechanism of colorectal cancer (CRC) formation. However, whether they are biologically different and truly form a distinct subclass of CRC, is not known. This study shows that the gene expression profile of serrated and conventional CRCs differs from each others and that serrated CRCs are not only morphologically novel, but also biologically distinct subclass of CRC. Keywords: molecular classification

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Project description:Two DNA repair pathways, non-homologous end joining (NHEJ) and alternative end joining (A-EJ), are involved in V(D)J recombination and chromosome translocation. Previous studies reported distinct repair mechanisms for chromosome translocation, with NHEJ predominantly involved in human and A-EJ in mice. NHEJ depends on DNA-PKcs, a critical partner in synapsis formation and downstream component activation. While DNA-PKcs inhibition promotes chromosome translocations harboring microhomologies in mice, its synonymous effect in human is not known. We find partial DNA-PKcs inhibition in human cell lines leads to increased genome-wide translocations composed mostly of direct joints, indicating the continued involvement of dampened NHEJ in these processes. In contrast, complete DNA-PKcs inhibition and genetic inhibition DNA-PKcs kinase domain substantially increased microhomology-mediated end joining (MMEJ), thus bridging the two different translocation mechanisms between human and mice. Similar to a previous study on Ku70 deletion, DNA-PKcs deletion in G1/G0-phase mouse pro-B cell lines, impair the recombination of RAG1/2-mediated DNA double-strand breaks (DSBs). This DNA-PKcs-deficient repair mechanism exhibited reduced V(D)J recombination efficiency, increased end resection, decreased polymerase-mediated insertions, loss of recombination fidelity and generated relatively higher rates of chromosome translocation as a consequence of dysregulated coding and signal end joining. Our study underscores DNA-PKcs in suppressing illegitimate chromosome rearrangement in both species.

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