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- W3119067900 abstract "Abstract The α‐isozyme of diacylglycerol kinase (DGK) enhances cancer cell proliferation and, conversely, it promotes the nonresponsive immune state known as T‐cell anergy. Moreover, a DGKα‐selective inhibitor, CU‐3, induced cell death in cancer‐derived cells and simultaneously enhanced T‐cell interleukin‐2 production. In addition to DGKα, DGKζ is also known to induce T‐cell anergy. In the present study, we examined whether combined inhibition/silencing of DGKα and DGKζ synergistically enhanced T‐cell activity. Combined treatment with CU‐3 or DGKα‐small interfering RNA (siRNA) and DGKζ‐siRNA more potently enhanced T‐cell receptor‐crosslink‐dependent interleukin‐2 production in Jurkat T cells than treatment with either alone. Intriguingly, in addition to activating T cells, dual inhibition/silencing of DGKα and DGKζ synergistically reduced viability and increased caspase 3/7 activity in AKI melanoma cells. Taken together, these results indicate that combined inhibition/silencing of DGKα and DGKζ simultaneously and synergistically enhances interleukin‐2 production in T cells and induces cell death in melanoma. Therefore, dual inhibition/silencing of these DGK isozymes represents an ideal therapy that potently attenuates cancer cell proliferation and simultaneously enhances immune responses that impact anticancer immunity." @default.
- W3119067900 created "2021-01-18" @default.
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- W3119067900 date "2021-01-05" @default.
- W3119067900 modified "2023-10-16" @default.
- W3119067900 title "Combined inhibition/silencing of diacylglycerol kinase α and ζ simultaneously and synergistically enhances interleukin‐2 production in T cells and induces cell death of melanoma cells" @default.
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- W3119067900 doi "https://doi.org/10.1002/jcb.29876" @default.
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