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FAM135B deficiency inhibits cytotoxic T cell activity in triple-negative breast cancer by blocking the IFI16-dependent STING pathway

ABSTRACT: FAM135B interacts with IFI16, inhibiting its ubiquitination and proteasomal degradation by competitively blocking its binding to the E3 ligase TRIM21, thereby initiating the IFI16-dependent STING signaling, ultimately leading to increased cytotoxic T cell activity.

ORGANISM(S): Homo Sapiens

SUBMITTER: Guangyu Yao

PROVIDER: PXD068216 | iProX | Tue Sep 09 00:00:00 BST 2025

REPOSITORIES: iProX

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FAM135B Deficiency Inhibits Cytotoxic T-cell Activity in Triple-Negative Breast Cancer by Blocking the IFI16-Dependent STING Pathway.

Lin Wanmei W Li Junze J Wu Jun J Huang Bin B Liang Junguang J Zhang Yuan Y Zhao Liang L Yao Guangyu G

Cancer immunology research 20260201 2

Immune checkpoint blockade (ICB) has improved outcomes for patients with several types of cancer. However, only a minority of patients with triple-negative breast cancer (TNBC) derive benefits, and the underlying mechanisms remain largely unknown. In this study, we identified family with sequence similarity 135 member B (FAM135B) as a regulator of antitumor immunity in TNBC. Single-cell sequencing data and functional assays demonstrated the critical role of FAM135B in activating cytotoxic T cell ...[more]

PMID: 41218197

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