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GCGR Loss-of-Function Mutations Promote Amino Acid-Dependent Pancreatic Neuroendocrine Tumor Initiation from a Subpopulation of Alpha Cells [single-cell RNA-seq]

ABSTRACT: Evaluating cell subpopulations in mouse pancreatic islets and pancreatic tumors

ORGANISM(S): Mus musculus

PROVIDER: GSE142233 | GEO | 2020/05/29

REPOSITORIES: GEO

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GCGR Loss-of-Function Mutations Promote Amino Acid-Dependent Pancreatic Neuroendocrine Tumor Initiation from a Subpopulation of Alpha Cells

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Elevated Serum Amino Acids Induce a Subpopulation of Alpha Cells to Initiate Pancreatic Neuroendocrine Tumor Formation.

Project description:The cellular origin of sporadic pancreatic neuroendocrine tumors (PNETs) is obscure. Hormone expression suggests that these tumors arise from glucagon-producing alpha cells or insulin-producing β cells, but instability in hormone expression prevents linage determination. We utilize loss of hepatic glucagon receptor (GCGR) signaling to drive alpha cell hyperproliferation and tumor formation to identify a cell of origin and dissect mechanisms that drive progression. Using a combination of genetically engineered Gcgr knockout mice and GCGR-inhibiting antibodies, we show that elevated plasma amino acids drive the appearance of a proliferative population of SLC38A5+ embryonic progenitor-like alpha cells in mice. Further, we characterize tumors from patients with rare bi-allelic germline GCGR loss-of-function variants and find prominent tumor-cell-associated expression of the SLC38A5 paralog SLC7A8 as well as markers of active mTOR signaling. Thus, progenitor cells arise from adult alpha cells in response to metabolic signals and, when inductive signals are chronically present, drive tumor initiation.

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