EVI5 unveils a role of the oncogene in modulating the Rab11/PD-L1 pathway in lung adenocarcinoma.

Ecotropic viral integration site 5 (EVI5), a member of the Tre-2/Bub2/Cdc16 (TBC) domain-containing protein family, has been implicated in the initiation of various cancers. However, its precise role in lung adenocarcinoma (LUAD) remains unclear. This study aimed to elucidate the function of EVI5 in LUAD, with a focus on its regulation of the immune checkpoint molecule PD-L1. In the present study, we found that EVI5, Rab11 and PD-L1 were significantly overexpressed in LUAD tissues compared to adjacent normal tissues. In vitro experiments demonstrated that EVI5 knockout suppressed the expression of Rab11 and PD-L1 in LUAD cells. Notably, EVI5 overexpression promotes the expression of Rab11 and PD-L1 in LUAD cells. EVI5 was also shown to interact with Rab11 to upregulate PD-L1 expression in LUAD cells. Mechanistically, our findings identify a novel EVI5-Rab11-PD-L1 axis and suggest that EVI5 is a potential regulator of the tumor immune microenvironment, which may have implications for the efficacy of immunotherapy.