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. 2021 Aug 2;23(9):979–992. doi: 10.1016/j.neo.2021.07.008

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© 2021 The Authors. Published by Elsevier Inc.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig 8 — Hypothetical model of p53-dependent interactions among INSM1, Cyclin D1 and Notch during PanNET tumorigenesis. (A) In PanNET cells with wild-type p53 and loss of MEN1, Notch signaling controls the expression of INSM1 and its localization to the nucleus. When cells are treated with GSI, Notch signaling is inhibited, causing INSM1 to localize in the cytoplasm, thereby decreasing Cyclin D1 transcription and blocking the cell cycle. (B) In PanNET cells with mutated p53 and loss of MEN1, INSM1 localization in the nucleus and proliferation is not influenced by the Notch pathway.