DPF3, a component of the SWI/SNF chromatin remodeling complex, is involved in various biological processes such as cell growth, proliferation, apoptosis, and motility. It is associated with multiple pathways, including TGF-β signaling, and plays a crucial role in maintaining normal cellular functions [2,3,5]. Genetic models, like KO/CKO mouse models, can be valuable for studying its functions.

In dendritic cells, a long non-coding RNA lnc-Dpf3, induced by CCR7 chemokine receptor stimulation, restrains DC migration by inhibiting HIF-1α-mediated glycolysis. DC-specific lnc-Dpf3 deficiency increases CCR7-mediated DC migration, leading to exaggerated adaptive immune responses and inflammatory injuries [1].

In clear cell renal cell carcinoma (ccRCC), the short isoform DPF3a promotes kidney cancer cell migration both in vitro and in vivo. DPF3a interacts with SNIP1, forms a complex with SMAD4 and p300 HAT, and activates cell movement-related genes [2].

In breast cancer, downregulation of DPF3 promotes the proliferation and motility of breast cancer cells through activating JAK2/STAT3 signaling [4]. Also, in renal cancer, germline variation in DPF3 can lead to reduced apoptosis and activation of the STAT3 pathway, and the risk allele at 14q24.2 activates a novel hypoxia-inducible transcription factor-binding enhancer of DPF3 expression, increasing the risk of developing renal cancer [5,6].

In conclusion, DPF3 is essential in regulating cell migration, proliferation, and apoptosis. Studies using KO/CKO mouse models and other loss-of-function experiments have revealed its significant roles in diseases such as cancer and inflammatory diseases. Understanding DPF3's functions provides insights into disease mechanisms and potential therapeutic targets for these conditions.