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Pancreatic Neoplasms: HELP
Articles by Lawrence Barerra
Based on 1 article published since 2009
(Why 1 article?)
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Between 2009 and 2019, Lawrence Barerra wrote the following article about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article S100A8 and S100A9 proteins form part of a paracrine feedback loop between pancreatic cancer cells and monocytes. 2018

Nedjadi, Taoufik / Evans, Anthony / Sheikh, Adnan / Barerra, Lawrence / Al-Ghamdi, Suliman / Oldfield, Lucy / Greenhalf, W / Neoptolemos, John P / Costello, Eithne. ·King Abdullah International Medical Research Centre, King Abdulaziz Medical City, Ministry of National Guard-Health Affairs, P. O. Box 9515, Jeddah, 21423, Saudi Arabia. nedjadita@ngha.med.sa. · Department of Molecular and Clinical Cancer Medicine, Institute of Translational Medicine, The University of Liverpool, Liverpool, UK. · King Abdullah International Medical Research Centre, King Abdulaziz Medical City, Ministry of National Guard-Health Affairs, P. O. Box 9515, Jeddah, 21423, Saudi Arabia. ·BMC Cancer · Pubmed #30558665.

ABSTRACT: BACKGROUND: The secretion of soluble factors enables communication between tumour cells and the surrounding microenvironment and plays an important role in oncogenesis. Pancreatic ductal adenocarcinoma (PDAC) is characterised by a highly reactive microenvironment, harbouring a variety of cell types, including S100A8/S100A9-expressing monocytes. S100A8/S100A9 proteins regulate the behaviour of cancer cells by inducing pre-metastatic cascades associated with cancer spread. The aim of this study was to examine how S100A8/A9 proteins mediate tumour-stroma crosstalk in PDAC. METHODS: Cytokine profiling of pancreatic cancer cell-derived conditioned media was performed using Bio-Plex Pro 27 Plex Human Cytokine assays. Protein expression and activation of downstream signalling effectors and NF-κB were assessed by western blotting analysis and reporter assays respectively. RESULTS: Stimulation of cultured pancreatic cancer cells with S100A8 and S100A9 increased the secretion of the pro-inflammatory cytokines IL-8, TNF-α, and FGF. S100A8, but not S100A9 induced PDGF secretion. Conversely, pancreatic cancer cell-derived conditioned media and the individual cytokines, TNF-α and TGF-β induced the expression of S100A8 and S100A9 proteins in the HL-60 monocytic cell line and primary human monocytes, while FGF and IL-8 induced the expression of S100A9 only. S100A8 and S100A9 activated MAPK and NF-κB signalling in pancreatic cancer. This was partially mediated via activation of the receptor of advanced glycosylation end-product (RAGE). CONCLUSION: S100A8 and S100A9 proteins induce specific cytokine secretion from PDAC cells, which in turn enhances the expression of S100A8/A9. This paracrine crosstalk could have implications for PDAC invasiveness and metastatic potential.