IFIT3 (Interferon Induced Protein With Tetratricopeptide Repeats 3)

Furthermore, CARTM4SF1-EVs synergized with Immune Checkpoint Blockade (ICB) therapy, leading to durable antitumor immune memory. Collectively, these findings establish CARTM4SF1-EVs therapy as a safe and effective strategy for targeted cancer immunotherapy, underscoring its potential for clinical application.

TM4SF1 may serve as a potential prognostic biomarker and therapeutic target for cervical cancer.

YBX1 stabilizes TM4SF1 mRNA via m5C modification in BCa, activating β- catenin/c-Myc signaling to drive tumor growth and glycolysis. This reveals a novel therapeutic target for BCa.

Together these findings implicate disease-specific vascular cells in PAH progression and suggest that TM4SF1 may be a novel therapeutic target for arterial remodeling.

Pathway BMDs were also calculated for Caco-2 (systemic lupus erythematosus, 9.7-18 μg/L; alcoholism, 9.7-20 μg/L; viral carcinogenesis, 9.3-18.1 μg/L), and HepG2 (metabolic pathways, 50-60 μg/L) cells. These findings highlight TPD-seq as an efficient workflow to yield quantitative and mechanistic data relevant for human health risk assessment.

TM4SF1 promotes HF progression and HSC activation by binding to and activating c-Src. TM4SF1 could be a future therapeutic target for HF by inhibiting HSC activation.

We also find enriched expression of TM4SF1, a transmembrane protein, in HV tumor cells. Chimeric antigen receptor (CAR) T cells engineered against TM4SF1 protein demonstrated in vitro and in vivo activity against bladder cancer cell lines in a TM4SF1 expression-dependent manner, highlighting its potential as a therapeutic target.

TM4SF1 was highly expressed in TECs undergoing the EMT and is thought to be linked to MVI. TECs with elevated TM4SF1 expression facilitate MVI during HCC via an effect on the EMT, suggesting the potential of TM4SF1 as a therapeutic target.

Targeting TM4SF1 via AAV induced tumor senescence, reduced tumor burden and synergistically enhanced the efficacy of anti-PD-1 therapy. Our results revealed that TM4SF1 regulated tumor cell senescence and immune evasion through the AKT pathway, highlighting its potential as a therapeutic target in HCC, particularly in combination with first-line immunotherapy.