The immunological comparison of control PDA tumors and Krt19-edited PDA tumors
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA794150 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17430130.fastq.gz | Fastqsanger.gz | |||
| SRR17430131.fastq.gz | Fastqsanger.gz | |||
| SRR17430132.fastq.gz | Fastqsanger.gz | |||
| SRR17430133.fastq.gz | Fastqsanger.gz | |||
| SRR17430134.fastq.gz | Fastqsanger.gz |
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Project description:Our studies indicate that cancer cells of carcinomas are coated with CXCL12 chemokine in covalent conjugation with keratin-19 (KRT19). Murine pancreatic ductal adenocarcinomas (PDA) formed with Krt19-edited cancer cells lack the CXCL12-coating and are infiltrated with T cells, compared to tumors formed with control sgScramble PDA cells. To probe the immunological role of this CXCL12-coating thoroughly, bulk RNA sequencing of subcutaneous (s/c) murine sgScramble PDA tumors and Krt19-edited PDA tumors were conducted.
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Project description:Our studies indicate that cancer cells of carcinomas are coated with CXCL12 chemokine in covalent conjugation with keratin-19 (KRT19). Murine pancreatic ductal adenocarcinomas (PDA) formed with Krt19-edited cancer cells lack the CXCL12-coating and are infiltrated with T cells, compared to tumors formed with control sgScramble PDA cells. To probe the immunological role of this CXCL12-coating thoroughly, bulk RNA sequencing of subcutaneous (s/c) murine sgScramble PDA tumors and Krt19-edited PDA tumors were conducted. As comparison, an immunogenic tumor model was also assessed. To do so, s/c sgScramble PDA tumors and PDA tumors formed with sgScramble cells exppressing doxcycline-inducible ovalbumin (icOVA) were harvested and processed for bulk RNA sequencing.
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Project description:The immunological comparison of control PDA tumors and Krt19-edited PDA tumors
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Project description:T cells exclusion precludes checkpoint inhibition efficacy in pancreatic ductal adenocarcinoma (PDA) and is mediated by the interaction between T cell CXCR4, and its ligand CXCL12, which is complexed to keratin-19 (KRT19) on the surface of PDA cells. KRT19 secretion is essential to this process but is unusual because KRT19 lacks an endoplasmic reticulum (ER)-directing signal peptide (SP). By using ER-restricted TurboID sys-tems and a split-GFP assay, we demonstrate that KRT19 enters the ER via its “head” domain. In vivo, tumors formed with ER-TurboID cells contain biotinylated KRT19. Additionally, KRT19 is shown to interact with the sig-nal recognition particle and its secretion is sensitive to canonical protein secretion inhibitors. Although keratin-8 (KRT8) co-localizes with KRT19 on the surface of PDA cells, KRT8 does not enter the ER. However, both keratins are externalized via secretory autophagy. Thus, despite lacking a classical SP, PDA cells secrete KRT19 to protect against immune attack.
2025-06-16 | PXD051583 | Pride
Project description:As a member of the acidic type I cytokeratin family, keratin 19 (KRT19) is originally known to form the intermediate filament cytoskeleton and responsible for structural rigidity and multipurpose scaffolds.KRT19 is abnormally expressed in various cancers including hepatocellular carcinoma, breast cancer,serous ovarian cystadenocarcinoma and et.al. KRT19 has been revealed to mediate cell cycle, cancer stem cell reprogramming by interacting with cellular molecules including receptors, adaptors, effectors and kinases. Increasing evidence illustrates the clinical significance of KRT19 in lung cancer, extensive studies are urged to elucidate the role and underlying mechanism of KRT19 in NSCLC progression, we performed RNA-Seq to identify its target genes in A549 cell lines.
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Project description:Pancreatic ductal adenocarcinoma (PDA) carries a dismal prognosis and current treatments are only modestly effective. We present evidence that this variation is caused in part by recurrent, pervasive molecular differences between tumors. mRNA expression profiles measured using microdissected PDA clinical samples reveal three dominant subtypes of disease; epithelial, mesenchymal and acinar-like. The classical and quasi-mesenchymal subtypes are observed in human and mouse PDA cell lines. Importantly, responses to cytotoxics and KRAS depletion in human PDA cell lines differ substantially between subtypes, and in opposing directions. Integrated genomics implicate and functional studies support overexpression of the trancription factor GATA6 as a driver of the epithelial subtype. These results provide a molecular framework for evaluating the prospects of personalized treatment in PDA. RNA was extracted from archival patient FFPE PDA samples and hybridized on Affymetrix U133 plus 2.0 microarrays. The CEL files were processed using R based Bioconductor and normalized values were obtained using RMA. RNA was extracted from human PDA cell line samples and hybridized on Affymetrix U133 plus 2.0 microarrays. The CEL files were processed using R based Bioconductor and normalized values were obtained using RMA. RNA was extracted from mouse PDA cell lines and hybridized on Affymetrix Mouse 430a 2.0 microarrays. The CEL files were processed using R based Bioconductor and normalized values were obtained using RMA.
2011-04-01 | E-GEOD-17891 | biostudies-arrayexpress
Project description:As a member of the acidic type I cytokeratin family, keratin 19 (KRT19) is originally known to form the intermediate filament cytoskeleton and responsible for structural rigidity and multipurpose scaffolds.KRT19 is abnormally expressed in various cancers including hepatocellular carcinoma, breast cancer,serous ovarian cystadenocarcinoma and et.al. KRT19 has been revealed to mediate cell cycle arrest, cancer stem cell reprogramming by interacting with cellular molecules including receptors, adaptors, effectors and kinases. Increasing evidence illustrates the clinical significance of KRT19 in lung cancer, extensive studies are urged to elucidate the role and underlying mechanism of KRT19 in NSCLC progression, we performed RNA-Seq to identify its target genes in PC-9 cell lines.
2026-01-21 | GSE299060 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDA) carries a dismal prognosis and current treatments are only modestly effective. We present evidence that this variation is caused in part by recurrent, pervasive molecular differences between tumors. mRNA expression profiles measured using microdissected PDA clinical samples reveal three dominant subtypes of disease; epithelial, mesenchymal and acinar-like. The classical and quasi-mesenchymal subtypes are observed in human and mouse PDA cell lines. Importantly, responses to cytotoxics and KRAS depletion in human PDA cell lines differ substantially between subtypes, and in opposing directions. Integrated genomics implicate and functional studies support overexpression of the trancription factor GATA6 as a driver of the epithelial subtype. These results provide a molecular framework for evaluating the prospects of personalized treatment in PDA.
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Project description:Here, using the mouse KRT19-deficient (sgKRT19-edited) PDA model, we find that intratumoral accumulation of natural killer T (NKT) cells are required to establish an immunologically active TME. Mechanistically, intratumoral NKT cells facilitate type I interferon (IFN) production to initiate an anti-tumor adaptive immune response, and orchestrate the intratumoral infiltration of T cells, dendritic cells, natural killer cells and myeloid-derived suppressor cells. At the molecular level, NKT cells promote the production of type I IFN through the interaction of their CD40L with CD40 on myeloid cells. To evaluate the theraputical potential of these observations, we find that administration of folinic acid to mice bearing PDA increases NKT cells in the TME and improves their response to anti-PD-1 antibody treatment. In conclusion, NKT cells have an essential role in the immune response to mouse PDA and are potential targets for immunotherapy.
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Project description:Nail stem cells (NSCs) are crucial for nail growth and fingertip regeneration, yet their identity and regulatory mechanisms remain unclear. Here, we used single-cell RNA sequencing to construct a spatiotemporal landscape of nine clusters of human nail epithelial cells. Through analysis of their bidirectional differentiation, we identified a KRT19+ subpopulation capable of differentiating into both nail structure and peri-nail epithelium. Our findings reveal that SOX2-controlled WNT signaling is inhibited in the proximal nail matrix, activated in the distal nail matrix, and subsequently downregulated by SOX9 towards the nail bed, guiding the orderly OFF-ON-OFF regulation of KRT19+ NSC differentiation into nail structure epithelium. In vivo validation using mouse models and human samples confirmed the regenerative capacity of KRT19+ NSCs. This study is the first to identify KRT19+ NSCs using a human nail single-cell atlas and elucidate their key regulatory mechanisms, providing a foundation for nail and digit regeneration therapies.
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