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Microbial changes in early pancreatic cancer progression

ABSTRACT: Microbial changes in early pancreatic cancer progression

PROVIDER: PRJEB33219 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3400200.fastq.gz	Fastqsanger.gz
	ERR3400210.fastq.gz	Fastqsanger.gz
	ERR3400220.fastq.gz	Fastqsanger.gz
	ERR3400230.fastq.gz	Fastqsanger.gz
	ERR3400240.fastq.gz	Fastqsanger.gz

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Microbial changes in early pancreatic cancer progression

Project description:Pancreatic cancer is among the deadliest cancers that affects almost 54,000 patients in United States alone, with 90% of them succumbing to the disease. Lack of early detection is considered to be the foremost reason for such dismal survival rates. Our study shows that resident gut microbiota is altered at the early stages of tumorigenesis much before development of observable tumors in a spontaneous, genetically engineered mouse model for pancreatic cancer. In the current study, we analyzed the microbiome of in a genetic mouse model for PDAC (KRASG12DTP53R172HPdxCre or KPC) and age-matched controls using WGS at very early time points of tumorigenesis. During these time points, the KPC mice do not show any detectable tumors in their pancreas. Our results show that at these early time points, the histological changes in the pancreas correspond to a significant change in certain gut microbial population. Our predictive metabolomic analysis on the identified bacterial species reveal that the primary microbial metabolites involved in progression and development of PDAC tumors are involved in polyamine metabolism.

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Induced Pluripotent Stem Cells From Pancreatic Ductal Adenocarcinoma Can Recapitulate Early Developmental Stages of Cancer

Project description:Pancreatic ductal adenocarcinoma (PDAC) has one of the worst prognoses of any human malignancy and there are few human cellular models of disease progression. When human PDAC cells are injected into immunodeficient animals, they create tumors of the late stage from which they were derived. We hypothesized that if human pancreatic cancer cells were converted to pluripotency and then allowed to differentiate back into pancreas, the developmental progression would recapitulate early stages of the cancer. To that end, we have generated isogenic matched sets of induced pluripotent stem (iPS) cell-like lines from epithelial cells of human pancreatic tumors and from histologically normal epithelial cells at the resected pancreatic margins. Notably, when injected into immunodeficient mice, at low or high passages, a human pancreatic cancer iPS-like line, but not the corresponding margin iPS-like line, slowly generates intra-epithelial neoplasia (PanIN) ductal structures that typically reflect the early stages of human pancreatic cancer. The PanIN-like ducts can be isolated and cultured. They secrete protein products reflective of PanINs and provide new insights into underlying regulatory networks. An additional iPS-like line from histologically normal cells at a pancreatic resection margin, but containing a mutation that predisposes to PDAC, does not generate PanIN ductal structures. These studies demonstrate that iPS technology can be exploited to recapitulate early progression events of a human epithelial cancer. Study includes a single experiment (#10): a tumor-adjacent pancreatic tissue control (10N); tumor tissue (10C); IPS-transformed tissue control (10N12); and IPS-transformed tumor tissue (10C22).

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NADPH Oxidase 1 in Chronic Pancreatitis-Activated Pancreatic Stellate Cells Facilitates the Progression of Pancreatic Cancer

Project description:Aims: Patients suffering from chronic pancreatitis (CP) have a higher risk of pancreatic ductal adenocarcinoma (PDAC). NADPH oxidase 1 (Nox1) in activated pancreatic stellate cells from a CP mouse model (CP-activated PaSCs) forms fibrotic tissue and up-regulates matrix metalloproteinase (MMP) 9. Yet, the role and mechanism of Nox1 in CP-activated PaSCs in the progression of PDAC is unknown. 1) We tested the ability of Nox1 in CP-activated PaSCs to facilitate the growth and invasion of pancreatic cancer cells. 2) We identified proteins in the secretome of CP-activated PaSCs whose production was Nox1-dependent. Results: In vitro, Nox1 in CP-activated PaSCs facilitated the migration/invasion of MIA PaCa-2 and HPAC cells. Nox1 evoked a both pro-invasive and cancer-promoting phenotype in PaSCs via a paracrine activation of both p38 MAPK and STAT3 pathways in neoplastic cells. In vivo, Nox1 in CP-activated PaSCs facilitated tumor growth, metastasis formation, and stromal expansion. Using mass spectrometry, we identified proteins protecting from cellular stresses in the secretome of CP-activated PaSCs whose production was Nox1-dependent. Innovation: Inhibiting the stromal Nox1 signaling at early stages can reduce the reorganization of histological barriers, and the protection of neoplastic cells from cellular stresses, ameliorating the progression of PDAC. Conclusions: Nox1 in CP-activated PaSCs induced both Twist1 and MMP-9 expression, causing changes in the extracellular matrix composition. In addition, Nox1 oxidized peroxiredoxins 1 and 4 through thioredoxin reductase 1, causing p38 MAPK and STAT3 phosphorylation in neoplastic cells when they were secreted from CP-activated PaSCs. Both mechanisms facilitated the progression of PDAC.

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