Journal of Translational Medicine · 2016 · 24 citations · 69 references
MedicineImmunologyOncologyCancer ImmunologyImmunotherapyTumor ImmunologyCancer ImmunotherapyCheckpoint Inhibitor TherapyCombination ImmunotherapyImmune Checkpoint RegulationImmunotherapy For Skin CancerTumor Microenvironment ModulationImmune Checkpoint Blockade ResistanceImmune Checkpoint ResistanceMek InhibitionMek InhibitorsMelanoma ImmunotherapyResistance To Checkpoint InhibitorsResistance To Immune Checkpoint InhibitionResponse To Immunotherapy
The PI3K/AKT/mTOR signaling pathway has been implicated in multiple cancers, and as a regulator of many key oncogenic processes. Our studies implicate a role for this pathway in resistance to both targeted and immune therapies for melanoma. Materials and methods: Melanoma cell lines and clinical specimens were utilized to study the significance and functional consequences of the PI3K/AKT/mTOR pathway. Analyses of clinical specimens were performed under institution review board-approved protocols. Results: Pilot whole genome expression profiling and synthetic lethality screens implicated oxidative phosphorylation (OxPhos) in resistance to BRAF and MEK inhibitors in BRAF-mutant human melanoma cell lines. Characterization of panels of human cell lines with de novo or acquired resistance to MAPK pathway inhibitors demonstrated that ~50 % of the cell lines exhibited a high OxPhos phenotype. The presence of high OxPhos correlated with increased expression of PGC1-alpha and with sensitivity to combined inhibition of the MAPK pathway and mTORC1/2. mTORC1/2 inhibition caused cytoplasmic sequestration of MITF and subsequent decreased expression of MITF-regulated genes, including PGC1-alpha. In vitro testing demonstrated that a direct OxPhos inhibitor similarly achieved growth inhibition and apoptosis in some human melanoma cell lines with high OxPhos. Further, the OxPhos inhibitor abrogated the growth of inhibitor-resistant BRAF mutant human melanoma cell lines in vivo. Activation of the PI3K/AKT/mTOR pathway by loss of PTEN was also shown to promote resistance to T cell mediated cell killing in vitro and in vivo. Loss of PTEN correlated with decreased CD8 cell infiltrates in clinical specimens and increased expression of immunosuppressive cytokines. While pan-PI3K inhibitors inhibited immune cell viability and function, isoform-selective inhibitors did not significantly affect immune function and they produced synergy with immunotherapy. Conclusions: The PI3K/AKT/mTOR signaling pathway is an important regulator of key cellular processes in melanoma, and should be considered as a candidate combinatorial partner for both targeted and immune therapies.
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