Extracellular vesicle-mediated EBAG9 transfer from cancer cells to tumor microenvironment promotes immune escape and tumor progression.

ABSTRACT: The antitumor immune response is a critical defense system that eliminates malignant cells. The failure of the system results in immune escape and proceeds to tumor growth. We have previously showed that estrogen receptor-binding fragment-associated antigen 9 (EBAG9) is a relevant cancer biomarker and facilities immune escape of cancers from the immune surveillance. EBAG9 in cancer cells suppresses T-cell infiltration into tumor in vivo, whereas that in host immune cells functions as a limiter for T-cell cytotoxicity. Considering that EBAG9 plays immune suppressive roles in both tumor and microenvironment, we here questioned whether EBAG9 is a transferable protein from cancer to surrounding T cells and affects antitumor immune response. In this study, we showed that spontaneous development

SUBMITTER: Miyazaki T 

PROVIDER: S-EPMC5833691 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature