Tumor-Associated Macrophage-Derived Exosomal LINC01232 Induces the Immune Escape in Glioma by Decreasing Surface MHC-I Expression.

ABSTRACT: Tumor-associated macrophage (TAM) infiltration facilitates glioma malignancy, but the underlying mechanisms remain unclear. Herein, it is reported that TAMs secrete exosomal LINC01232 to induce tumor immune escape. Mechanistically, LINC01232 is found to directly bind E2F2 and promote E2F2 entry into the nucleus; the two synergistically promots the transcription of NBR1. The increase in binding between NBR1 binding and the ubiquitinating MHC-I protein through the ubiquitin domain causes an increase in the degradation of MHC-I in autophagolysosomes and a decrease in the expression of MHC-I on the surface of tumor cells, which in turn led to tumor cell escape from CD8⁺ CTL immune attack. Disruption of E2F2/NBR1/MHC-I signaling with shRNAs or blockade with the corresponding antibodi

SUBMITTER: Li J 

PROVIDER: S-EPMC10265094 | biostudies-literature | 2023 Jun

REPOSITORIES: biostudies-literature