A novel mechanism published for PIM kinases to enhance cell motility

In our article published Aug 8, 2020 in Cell Communication and Signaling, we describe actin capping proteins as novel PIM substrates. We have found several PIM target sites from both subunits of the heterodimeric capping proteins, and demonstrate that phosphorylation reduces their ability to protect actin filament ends from disassembly, leading to enhanced cell motility. By contrast, PIM inhibitors or capping protein mutations have opposite effects, restricting actin-dependent cellular movements. These results are of interest, as they help to explain how PIM kinases enhance the motility and metastatic growth of cancer cells, and thereby support the development of PIM-targeted therapies to treat patients with solid tumors.

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