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- W4247031871 abstract "Abstract Background : N-cadherin is a major regulatory factor of epithelial-to-mesenchymal transition (EMT), and the association and coordination of EMT and neuroendocrine differentiation (NED) with immunosuppression have been reported in several tumor types. Therefore, we hypothesize that N-cadherin may play vital role in this process. Methods : We performed human tissue studies, cell-level explorations and in vivo experiments to determine the statuses of N-cadherin and immune checkpoint proteins (PD-L1 and IDO-1) to verify the co-expression of these biomarkers. Then, we used tumor-bearing mice to test the treatment effect of N-cadherin deletion. Moreover, the mechanism by which N-cadherin regulates PD-L1/IDO-1 expression was also assessed. Results : According to our data, N-cadherin expression is necessary for PD-L1 expression and dramatically increases the expression of IDO-1 through an IFN- response. On the contrary, IDO-1 and PD-L1 can prompt EMT. N-cadherin knockout completely reverses this process. The core mechanism underlying these phenomena is that N-cadherin causes JAK1 to be re-expressed in cells with genomic JAK1 loss via the active EMT/immunosuppression positive feedback loop. Conclusion : These data indicate that N-cadherin can regulate the EMT/immunosuppression positive feed loop. Preclinical research has shown that N-cadherin deletion promotes the development of antitumor responses by decreasing immunosuppression." @default.
- W4247031871 created "2022-05-12" @default.
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- W4247031871 date "2020-07-17" @default.
- W4247031871 modified "2023-10-17" @default.
- W4247031871 title "New Immunotherapy Biomarker N-Cadherin Rescue Immunosuppress Caused by PD-L1/IDO-1 in Prostate Cancer" @default.
- W4247031871 doi "https://doi.org/10.21203/rs.3.rs-42523/v1" @default.
- W4247031871 hasPublicationYear "2020" @default.
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