Ontology highlight
ABSTRACT:
PROVIDER: PRJEB60909 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 139273_new.g.vcf.csi | Other | |||
| 139273_new.g.vcf.gz | Vcf | |||
| 139273_chromY.g.vcf.csi | Other | |||
| 139273_chromY.g.vcf.gz | Vcf | |||
| Dutch_Genebank_Cattle_merged.vcf.csi | Other |
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Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies for its difficult early diagnosis and poor prognosis. The molecular determinants dictating pancreatic cancer initiation and progression remain to be defined and are essential to its effective early detection and successful treatment. Little is known on the cingulin (CGN) expression and function in carcinogenesis. In this study, we demonstrate the critical oncogenic role of CGN in PDAC pathogenesis. Increased expression of CGN promoted pancreatic acinar-to-ductal metaplasia (ADM) and CGN is progressively upregulated during pancreatic cancer initiation and progression. CGN was required for pancreatic cancer cell proliferation, gemcitabine resistance, tumorigenesis and invasion and its overexpression predicted a poor patient prognosis. Mechanistically, CGN enhanced EGFR/AXL/ERK signaling pathway through increasing the mRNA stabilization and the protein expression of nuclear-cytoplasmic transport protein, importin-7 (IPO7) and the nuclear translocation of pERK, thus promoting the malignant behaviors of PDAC cells. Therefore, our study has demonstrated that CGN forms a novel oncogenic signaling axis, which could be an effective therapeutic target for PDAC treatment.
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Project description:Mucosal-associated invariant T (MAIT) cells have been implicated in various inflammatory diseases of barrier organs, but so far, their role in kidney disease is unclear. Here we report that MAIT cells that recognize their prototypical ligand, the vitamin B2 intermediate 5-OP-RU presented by MR1, reside in human and mouse kidneys. Single cell RNAseq analysis reveals several intrarenal MAIT subsets, and one, carrying the genetic fingerprint of tissue-resident MAIT17 cells, is activated and expanded in a murine model of crescentic glomerulonephritis (cGN). An equivalent subset is also present in kidney biopsies of patients with anti-neutrophil cytoplasmatic antibody (ANCA)-associated cGN. MAIT cell-deficient MR1 mice show aggravated disease, whereas B6-MAITCAST mice, harboring higher MAIT cell numbers, are protected from cGN. The expanded MAIT17 cells express anti-inflammatory mediators known to suppress cGN, such as CTLA-4, PD-1, and TGF-β. Interactome analysis predicts CXCR6 – CXCL16-mediated cross-talk with renal mononuclear phagocytes, known to drive cGN progression. In line, we find that cGN is aggravated upon CXCL16 blockade. Finally, we present an optimized 5-OP-RU synthesis method which we apply to attenuating cGN in mice. In summary, we propose that CXCR6+ MAIT cells might play a protective role in cGN, implicating them as a potential target for anti-inflammatory therapies.
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