Fig. 8

TMEM160 promotes immune escape and radiotherapy resistance to colorectal cancer cells by binding to PD-L1. In the context of CRC, the interaction between membrane-localized PD-L1 and PD-1 on T cells plays a critical role in inhibiting T cell activation. When the expression of TMEM160 is low, PD-L1 can bind to SPOP, which triggers the proteasomal degradation of PD-L1. As a result, the expression of PD-L1 localized as the cellular membrane decreased, ultimately promoting T cell activation. Conversely, when TMEM160 expression was increased in vivo, the binding of TMEM160 to PD-L1 increased, so that the binding of PD-L1 to SPOP decreased, resulting in a decrease in PD-L1 ubiquitination and stabilizing its expression, leading to immune escape and radiotherapy resistance in CRC cells. This suggests that TMEM160 expression levels can impact the stability and localization of PD-L1, ultimately influencing immune regulation and the response to radiotherapy in CRC. The figure was drawn using Figdraw