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Erener, S. ; Ellis, C.E.* ; Ramzy, A.* ; Glavas, M.M.* ; O'Dwyer, S.* ; Pereira, S.* ; Wang, T.* ; Pang, J.* ; Bruin, J.E.* ; Riedel, M.J.* ; Baker, R.K.* ; Webber, T.D.* ; Lesina, M.* ; Blüher, M. ; Algül, H.* ; Kopp, J.L.* ; Herzig, S. ; Kieffer, T.J.*

Deletion of pancreas-specific miR-216a reduces beta-cell mass and inhibits pancreatic cancer progression in mice.

Cell Rep. Med. 2:100434 (2021)

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miRNAs have crucial functions in many biological processes and are candidate biomarkers of disease. Here, we show that miR-216a is a conserved, pancreas-specific miRNA with important roles in pancreatic islet and acinar cells. Deletion of miR-216a in mice leads to a reduction in islet size, β-cell mass, and insulin levels. Single-cell RNA sequencing reveals a subpopulation of β-cells with upregulated acinar cell markers under a high-fat diet. miR-216a is induced by TGF-β signaling, and inhibition of miR-216a increases apoptosis and decreases cell proliferation in pancreatic cells. Deletion of miR-216a in the pancreatic cancer-prone mouse line KrasG12D;Ptf1aCreER reduces the propensity of pancreatic cancer precursor lesions. Notably, circulating miR-216a levels are elevated in both mice and humans with pancreatic cancer. Collectively, our study gives insights into how β-cell mass and acinar cell growth are modulated by a pancreas-specific miRNA and also suggests miR-216a as a potential biomarker for diagnosis of pancreatic diseases.

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Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Biomarker ; Circulating Mirna ; Diabetes ; Micro-rna ; Mir-216a ; Pancreatic Cancer ; Pdac ; β-cell Mass

ISSN (print) / ISBN 2666-3791

e-ISSN 2666-3791

Journal Cell Reports Medicine

Quellenangaben Volume: 2, Issue: 11, Article Number: 100434

Publisher Cell Press

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Institute of Diabetes and Cancer (IDC)
Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)