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The EVI5 oncogene drives tumor immune escape by regulating PD-L1 in Lung Adenocarcinoma

ABSTRACT: 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 investigated the pro-tumoral role of EVI5 in LUAD, focusing on its regulation of PD-L1, a key molecule involved in tumor immune evasion. In the present study, EVI5 was significantly overexpressed in LUAD tissues compared to adjacent normal tissues. In vitro experiments demonstrated that EVI5 knockout suppressed tumor immune escape. Notably, EVI5 overexpression promotes immune evasion by interacting with Rab11. Mechanistically, EVI5 was found to regulate downstream signaling pathways through Rab11-mediated activation of PD-L1 in LUAD cells. These findings suggest that EVI5 plays a crucial role in modulating immune escape, and may influence the efficacy of immunotherapeutic agents.

ORGANISM(S): Homo Sapiens

SUBMITTER: Tingting Cai

PROVIDER: PXD064761 | iProX | Sat Jun 07 00:00:00 BST 2025

REPOSITORIES: iProX

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