FOXD1 expression

FOXD1 activates the glycolysis pathway by upregulating KIFC1, thereby facilitating BC cells' DDP resistance. Therefore, the FOXD1/KIFC1 axis linked the glycolysis pathway to DDP resistance and may be a promising new target for reinforcing DDP resistance in BC.

The study highlights FOXD1 as a key player in OSCC pathogenesis and a potential prognostic marker and therapeutic target, particularly when influenced by WPSC exposure. Further research is needed to explore FOXD1's molecular mechanisms and clinical implications to enhance OSCC treatment strategies.

Additionally, the biological mechanisms of FOXD1 based on FOXD1-related genomic spectrum, molecular pathways, tumor microenvironment, and drug treatment sensitivity were examined using The Cancer Genome Atlas (TCGA) database, aiming to reasonably explain why FOXD1 leads to poor prognosis of UVM. On these bases, a novel tumor prognostic model was established using the FOXD1-related immunomodulators TMEM173, TNFRSF4, TNFSF13, and ULBP1, which will enable the stratification of disease seriousness and clinical treatment for patients.

The effect of FOXD1 knockdown on PC cells was reversed by LMNB1 overexpression. In conclusion, FOXD1, positively regulated by LMNB1, served as an oncogene in PC and may be a potential biomarker and treatment target for PC.

Oxaliplatin resistance was assessed using CCK‑8 and apoptosis assays in vitro, and using a tumor xenograft model in vivo...Notably, inhibition of this pathway with a specific β‑catenin inhibitor (XAV‑939) could impair the effects induced by the overexpression of FOXD1. In summary, these results indicated that FOXD1 may promote cell stemness and the chemoresistance of CRC by binding directly to β‑catenin and enhancing β‑catenin nuclear localization; therefore, it may be considered a potential clinical target.

According to multivariate analysis, FOXD1 was an independent prognostic factor for OS and DFS. The results revealed that FOXD1 could be a prognostic factor for HNSCC and might serve as a potential target for novel therapies.

FOXD1 can be considred a diagnostic biomarker for OSCC. RE inhibits autophagy of oral human cancer cells via mTOR/LC3I/II-dependent pathways and decrease caspase -3 apoptotic level.

FOXD1 is a novel factor which could potentially be involved in the metastatic capacity of high-risk UM. Elucidating the function of FOXD1 in UM could provide insight into the malignant transformation of uveal melanocytes, especially in high-risk UM.

Our miRNA-based approach is an effective strategy for the identification of prognostic markers and therapeutic target molecules in HNSCC. Moreover, these findings led to insights into the molecular pathogenesis of HNSCC.

Our results suggest that silencing of FOXD1 suppresses metastatic potentials of the PCa via N-cadherin - Wnt/β-catenin crosstalk. Therefore, the expression status of FOXD1 may be a new prognostic factor as well as a potential therapeutic target in prostate cancer treatment.

The results showed that patients with high expression of both FOXD1 and Plk2 have the worst survival. A combination of FOXD1 and Plk2 can better evaluate patients' survival.