Meanwhile, low FOXD3 protein expression was significantly correlated with poor histopathological grading, lymph node metastasis, and poor prognosis of patients, indicating its potential as a tumor marker that may be of potential value as a therapeutic target for CRC.
These findings demonstrate that FOXD3 acts as a tumor suppressor during anaplastic thyroid carcinogenesis and highlight its potential for clinical application.
These findings suggest that FOXD3 plays a potential tumor suppressor role in NSCLC progression and represents a promising clinical prognostic marker and therapeutic target for this disease.
A greater number of patients with invasive, triple-negative breast cancer were also negative forFoxD3 expression than in other, non-triple-negative tumor types.
FOXD3-mediated transcriptional control of tumor suppressors is deregulated by H pylori infection-induced hypermethylation; this could perturb the balance between cell death and survival.
Our results indicate that FOXD3 exhibits tumor suppressive activity that affects the growth, aggressiveness and angiogenesis of NB through transcriptional regulation of NDRG1.