FOXD1 (Forkhead Box D1)

Our findings suggest CSRS score and its constituent genes represent potential biomarkers for prognosis and immunotherapeutic benefit in COAD patients. Extending this nine-gene set into a broader senescence-associated panel should be a next step toward delivering truly individualized treatment plans.

Clinically, circulating miRNA panels (e.g., miR-4257, miR-6785-5p, and miR-187-5p) enhance early detection, while miR-125a-5p boosts the trastuzumab response via ERBB2 targeting...This review highlights miRNAs as pivotal regulators in gastric carcinogenesis and promising precision medicine tools. The study findings will promote the standardization of profiling methods and accelerate translational research, both of which are essential to the advancement of GC diagnostic and therapeutic strategies.

Lymph node MSCs in DLBCL patients exhibit unique biological behavior and gene expression profiles, which may be closely related to clinical chemotherapy resistance.

The combination of sTE and RPH may offer a safe, cost-effective, and feasible alternative to TEM for treating LeREC, particularly in resource-limited settings. It facilitates wider clinical application without compromising curative efficacy.

Our study demonstrates that a mutually reinforcing FOXD1/NAT10 positive feedback loop drives NPC progression, providing new therapeutic vulnerabilities for clinical intervention.

Our study revealed for the first time that TAM-derived exosomes modulate m6A levels in SHH-MB, which promotes tumor progression via FOXD1. We identified FOXD1 as a novel therapeutic target whose inhibition sensitizes SHH-MB to immune checkpoint blockade.

Our study elucidated a novel function of FOXD1 in melanoma pathogenesis, highlighting its role in orchestrating the immunosuppressive TME by promoting the generation of MDSC via IL6 upregulation.

The six-mfrlncRNA signature is a new biomarker for forecasting prognosis and treatment response in cervical cancer.

Also, ANXA3 silencing could reduce lung cancer tumorigenesis and enhance DDP sensitivity by decreasing ANXA4 expression in vivo. ANXA3, activated by FOXD1, might contribute to the DDP resistance of lung cancer via regulating ANXA4, providing new ideas for overcoming chemoresistance in lung cancer.

In contrast, Foxd1-ENLT mutant kidneys exhibit expansion in renal capsule and cap mesenchyme, with dysregulated stromal gene expression affecting stroma-epithelium crosstalk. Our findings uncover distinct pathways through which ENL mutations disrupt nephrogenesis, providing a foundation for further investigations into their role in tumorigenesis.

ALG3 directly interacted with FOXD1 and induced this N-glycosylation. Targeting the ALG3/FOXD1/BNIP3 axis offers a promising therapeutic strategy to inhibit the progression of NPC, which highlighting the potential of therapeutics targeting ALG3 and FOXD1 for regulating mitophagy and overcoming GEM resistance.