Fig. 2

Targeting PKCδ inhibited the growth of tumor and enhanced intratumoral T cell diversity. A PKCδ^−/− cell model based on EGFR double mutated cell H1975. B MTT assay showed that compared with control group, PKCδ depletion remarkably suppressed growth of cancer cells. C Flow cytometry analysis demonstrated that combination of PKCδ inhibitor and EGFR TKI significantly enhanced apoptotic percentage of resistant cancer cells. D PKCδ activator PEP-005 activated PI3K-ERK signaling. E, F Flow cytometry results showed that knock out of PKCδ promoted infiltration of T cells into TME and increased release of cytokine IFN-γ from CD8⁺ T cells. G, H In vivo EGFR-mutated xenograft nude mice model, PKCδ^−/− remarkably decreased tumor weight and size. I, J After knockout PKCδ, the number of TILs detected by flow cytometer was increased significantly in TME and survival time of mice was prolonged. K ELISA assay proved that compared with control (normal lung epithelial cells, BEAS-2B), co-cultured with BEAS-2B overexpressed mutated EGFR^L858R+T790M, T cells activity was compromised and thus the secretion of IFN-γ was suppressed. Data was triplicated and represented as mean ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001)