Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 437, Issue 3, Pages 433-439Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2013.06.097
Keywords
Pancreatic cancer; Pancreatitis; Fibrosis; Stroma; MicroRNA
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Funding
- Japan Society for the Promotion of Science
- Pancreas Research Foundation of Japan
- Kanae Foundation for Life and Socio-Medical Science
- Uehara Memorial Foundation
- Astellas Foundation for Research on Metabolic Disorders
- Research Committee of Intractable Pancreatic Diseases by the Ministry of Health, Labour, and Welfare of Japan
- Grants-in-Aid for Scientific Research [23591008] Funding Source: KAKEN
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There is accumulating evidence that pancreatic stellate cells (PSCs) promote the progression of pancreatic cancer. microRNAs (miRNAs) are small non-coding RNAs acting as negative regulators of gene expression at the post-transcriptional level. This study aimed to clarify the role of miRNAs in the interaction between PSCs and pancreatic cancer cells. Pancreatic cancer cells were mono-cultured or indirectly co-cultured with PSCs. miRNAs were prepared, and Agilent's miRNA microarray containing probes for 904 human miRNAs was used to identify differentially expressed miRNAs. miR-210 was identified as an upregulated miRNA by co-culture with PSCs. Conditioned media of PSCs activated ERK and Akt, but not hypoxia-inducible factor-1 alpha pathway. PSCs-induced miR-210 upregulation was inhibited by inhibitors of ERR and PI3K/Akt pathways. Inhibition of miR-210 expression decreased migration, decreased the expression of vimentin and snai-1, and increased the membrane-associated expression of beta-catenin in Panc-1 cells co-cultured with PSCs. In conclusion, our results suggest a novel role of miR-210 in the interaction between PSCs and pancreatic cancer cells. (C) 2013 Elsevier Inc. All rights reserved.
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