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- W4387445987 abstract "Abstract Conventional chemotherapy- and radiotherapy-induced cancer senescence, which is characterized by poor proliferation, drug resistance, and SASP, has gained attention as contributing to cancer relapse and the development of an immunosuppressive TME. However, the association between cancer senescence and anti-tumor immunity remains largely unknown. Here, we found that senescent cancer cells increase the level of PD-L1 by promoting its glycosylation and identified RPN1 as the major glycosyltransferase of PD-L1 during cancer senescence. RPN1 depletion significantly reduced this elevated level of PD-L1 through the ERLAD pathway to increase the susceptibility of senescent cancer cells to T-cell-mediated killing. Consistently, RPN1 depletion suppressed recurrence by decreasing PD-L1 levels and boosting CTL activity. Moreover, anti-PD-1 therapy effectively reduced the number of senescent cancer cells in irradiated tumors. These results provide crucial insights into how senescent cancer cells can escape T-cell immunity following cancer treatment and thereby contribute to cancer recurrence. Our findings also highlight the therapeutic promise of senescent cancer cell targeting for cancer treatment." @default.
- W4387445987 created "2023-10-10" @default.
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- W4387445987 date "2023-10-09" @default.
- W4387445987 modified "2023-10-11" @default.
- W4387445987 title "Therapy-induced senescent cancer cells contribute to cancer recurrence by providing a PD-L1 umbrella regulated by ribophorin 1" @default.
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- W4387445987 doi "https://doi.org/10.21203/rs.3.rs-3412374/v1" @default.
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