Inhibition of PAK1 suppresses pancreatic cancer by stimulation of anti-tumour immunity through down-regulation of PD-L1
Journal Title
Cancer Letters
Publication Type
Journal Article in press
Abstract
Immunotherapies have not yielded significant clinical benefits for pancreatic ductal adenocarcinoma (PDA) because of the existence of an immunosuppressive tumour microenvironment (TME) characterised by a desmoplastic stroma containing infiltrated immune cells and activated pancreatic stellate cells (PSCs). This study aims to investigate the involvement of PAK1 in anti-tumour immunity. In PDA patients low PAK1 expression, low activation of PSC and high CD8(+) T cell/PAK1 ratios correlated with longer overall survival. In a murine PDA model PAK1 knockout increased intra-tumoral CD4(+) and CD8(+) T cells, inhibited PSCs activation and extended survival. Inhibition of PAK1 reduced PSC-stimulated PDA cell proliferation and migration, blocked PSC-mediated protection of PDA cells from killing by cytotoxic lymphocytes and decreased intrinsic and PSC-stimulated PD-L1 expression in PDA cells, which further sensitized PDA cells to cytotoxic lymphocytes. Inhibition of PAK1 stimulates anti-tumour immunity by increasing intra-tumoral CD4(+) and CD8(+) T cells, and by sensitizing PDA cells to killing by cytotoxic lymphocytes via down-regulation of intrinsic and PSC-stimulated PD-L1 expression. PAK1 inhibitors, especially in combination with immune checkpoint inhibitors may result in improved efficacy of immunotherapy of PDA.
Publisher
Elsevier
Research Division(s)
Immunology
PubMed ID
31857154
Terms of Use/Rights Notice
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Creation Date: 2019-12-23 11:50:08
Last Modified: 2019-12-23 11:55:29
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