Tumor cell-intrinsic BIN1 deficiency promotes the immunosuppression and impedes ferroptosis of non-small cell lung cancer via G3BP1-mediated degradation of STAT1.

ABSTRACT:

Background

Tumors often evade immune surveillance by limiting T cell infiltration. In non-small cell lung cancer (NSCLC), increased infiltration of CD8⁺ T cells is associated with a favorable response to immunotherapy. While BIN1 is recognized as a tumor suppressor gene, its role in shaping the tumor microenvironment in NSCLC has yet to be fully clarified.

Methods

To investigate the relationship between BIN1 expression and CD8⁺T cell infiltration in NSCLC, we performed a comprehensive data analysis utilizing clinical information from NSCLC patients. BIN1 expression levels in NSCLC tissues were evaluated, and their correlation with CD8⁺T cells infiltration and patient survival outcomes was examined. Loss-of-function strategies targeting BIN1 w

SUBMITTER: Wang J 

PROVIDER: S-EPMC12063428 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature