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Insulin-like growth factor-binding protein 2 Induces Epithelial-mesenchymal Transition via Activation of NF-?B Pathway in Pancreatic Ductal Adenocarcinoma

ABSTRACT: IGFBP2 has been shown to act as an oncogene augmenting tumor progression in a number of malignancies. We sought to investigate role of IGFBP2 and its related pathways in PDAC. Gene expression profiling were used to reveal the key signaling pathways. Microarray experiments in IGFBP2-overexpressing AsPc-1 cells were carried out.Transcriptional profiling of human pancreatic cancer cells AsPc-1 comparing empty vector transfected control AsPc-1 cells with AsPc-1 cells transfected with pcDNA3.1-IGFBP2. We performed cDNA microarray analysis to compare IGFBP2 stably expressing cell line originating from AsPc-1 with empty vector control cells. AsPC-1 clones transfected with empty vector were placed in the reference channel in hybridization.

ORGANISM(S): Homo sapiens

SUBMITTER: Gao Song

PROVIDER: S-ECPF-GEOD-64611 | biostudies-other |

REPOSITORIES: biostudies-other

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Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive carcinoma entities worldwide with early and rapid dissemination. Recently, we discussed the role of microRNAs as epigenetic regulators of Epithelial-to-Mesenchymal Transition (EMT) in PDAC. In this study, we investigated their value as diagnostic and prognostic markers in tissue and blood samples of 185 patients including PDAC, non-malignant pancreatic disorders, and age-matched healthy controls. Expression of the microRNA-200-family (microRNAs -141, -200a, -200b, -200c, -429) and microRNA-148a was significantly downregulated in tissue of PDAC Union internationale contre le cancer (UICC) Stage II. Correspondingly, stromal PDAC tissue showed strong expression of Fibronectin, Vimentin, and ZEB-1 (Zinc finger E-box-binding homeobox) versus low expression of E-cadherin. Transient transfection of microRNA-200b and microRNA-200c mimics resulted in the downregulation of their key target ZEB-1. Inversely, blood serum analyses of patients with PDAC UICC Stages II, III, and IV showed a significant over-expression of microRNA-200-family members, microRNA-148a, microRNA-10b, and microRNA-34a. Correspondingly, Enzyme-linked Immunosorbent Assay (ELISA) analyses revealed a significant over-expression of soluble E-cadherin in serum samples of PDAC patients versus healthy controls. The best diagnostic accuracy to distinguish between PDAC and non-PDAC in this patient collective could be achieved in tissue by microRNA-148a with an area under the receiver-operating-characteristic (ROC) curve (AUC) of 0.885 and in blood serum by a panel of microRNA-141, -200b, -200c, and CA.19-9 with an AUC of 0.890. Both diagnostic tools outreach the diagnostic performance of the currently most common diagnostic biomarker CA.19-9 (AUC of 0.834). Kaplan Meier survival analysis of this patient collective revealed an improved overall survival in PDAC patients with high expression of tissue-related microRNA-34a, -141, -200b, -200c, and -429. In conclusion, EMT-regulating microRNAs have great potential as liquid and solid biopsy markers in PDAC patients. Their prognostic and therapeutic benefits remain important tasks for future studies.

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Insulin-like growth factor-binding protein 2 Induces Epithelial-mesenchymal Transition via Activation of NF-?B Pathway in Pancreatic Ductal Adenocarcinoma

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