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Wnt1 silences CC/CXC motif chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma

ABSTRACT: Wnt1 silences CC/CXC motif chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma

PROVIDER: PRJNA507436 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8257981.fastq.gz	Fastqsanger.gz
	SRR8257982.fastq.gz	Fastqsanger.gz
	SRR8257983.fastq.gz	Fastqsanger.gz
	SRR8257984.fastq.gz	Fastqsanger.gz
	SRR8257985.fastq.gz	Fastqsanger.gz

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Wnt1 silences CC/CXC motif chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma

Project description:This study showed that the oncogenic ligand Wnt1 silences chemokine genes in dendritic cells, leading to impaired cross-priming of T cells in lung adenocarcinoma. Blocking Wnt1 enhanced rejection of tumors by acting concomitantly at the cancer and immune cell level.

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Wnt1 silences CC/CXC motif chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma

Project description:Wnt1 silences CC/CXC motif chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma

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Wnt1 silences CC/CXC motif chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma

Project description:Lung adenocarcinoma (LUAD)-derived oncogenic Wnts increase cancer cell proliferative/stemness potential, but whether they also impact the immune microenvironment is unknown. Here we show that LUAD cells use paracrine Wnt1 signaling to induce immune resistance. Wnt1 correlated strongly with tolerogenic genes on the TCGA expression data. In another cohort, Wnt1 was inversely associated with T cell abundance. Altering Wnt1 expression profoundly affected growth of murine lung adenocarcinomas and this was strongly dependent on conventional dendritic cells and T cells. Mechanistically, Wnt1 lead to transcriptional silencing of CC/CXC chemokines in dendritic cells and T cell cross-tolerance. Wnt-target genes were up-regulated in human intratumoral dendritic cells and decreased upon silencing Wnt1, accompanied by enhanced T cell cytotoxicity. siWnt1-loaded nanoparticles as single therapy or part of combinatorial immunotherapies acted at both arms of the cancer-immune ecosystem to halt tumor growth. Collectively, our studies show that Wnt1 enhances adaptive immune rejection of lung adenocarcinomas and highlight its potential targeting as a novel therapeutic strategy

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Function of chemokine (CXC motif) ligand 12 in periodontal ligament fibroblasts

Project description:The periodontal ligament (PDL) is one of the connective tissues located between the tooth and bone. It is characterized by rapid turnover. Periodontal ligament fibroblasts (PDLFs) play major roles in the rapid turnover of the PDL. Microarray analysis of human PDLFs (HPDLFs) and human dermal fibroblasts (HDFs) revealed markedly high expression of chemokine (CXC motif) ligand 12 (CXCL12) in the HPDLFs, which plays an important role in the migration of mesenchymal stem cells (MSCs). The function of CXCL12 in the periodontal ligament was investigated in HPDLFs. CXCL12 in HPDLFs and HDFs was examined by microarray, RT-PCR, qRT-PCR and ELISA. It was also immunohistochemically examined in the PDL in vivo. Chemotactic ability of CXCL12 was evaluated both in PDLFs and HDFs with migration assay of MSCs. The expression of CXCL12 in the HPDLFs was much higher than that in HDFs in vitro. CXCL12 was localized in fibroblasts and extracellular matrix in the PDL in rats. Migration assay demonstrated that the number of migrated MSCs by HPDLFs was significantly higher than that by HDFs. In addition, the migrated MSCs also expressed CXCL12 and several genes that are familiar to fibroblasts. The results suggested that PDLFs are able to synthesize and secrete CXCL12 protein, and that CXCL12 induces migration of MSCs in the PDL in order to maintain rapid turnover of the PDL. The objective of this study was to investigate the function of CXCL12 in the PDL with rapid turnover.Microarray analysis was performed using a Whole Human Genome 8x60K (Agilent Technologies, Tokyo, Japan) containing approximately 44,000 transcripts. According to the manufacturerM-bM-^@M-^Ys protocol, total RNAs from HPDLFs and HDFs were labeled with Cy3 and hybridized on the microarray. The hybridization data for HPDLFs were compared with data for HDFs.

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