MBD3 (Methyl-CpG Binding Domain Protein 3)

Furthermore, MBD3 is transcriptionally regulated by bromodomain-containing protein 4 (BRD4), and MBD3 knockdown enhances the sensitivity of CRPC cells to BET inhibitors. These findings suggest that the BRD4-MBD3-PTEN axis is a new pathway in CRPC, with MBD3 representing a potential therapeutic target, particularly in combination with BET inhibitors.

We identified a novel function of lncRNA16 in inhibiting pyroptosis and proposed an effective therapeutic drug, the miRNA1827 agomir, for chemosensitization. This study offers a potential strategy for treating patients with NSCLC, especially those with platinum resistance.

MBD3 promoted migration, invasion, proliferation and EMT by upregulating ACTG1 via PI3K/AKT signaling activation in GC cells and may be a potential diagnostic and prognostic target.

Our findings were further confirmed by IHC analysis of the above proteins in HCC tissues before and after SBRT. Conclusions Our study suggests that SBRT can reprogram the tumor immune microenvironment by activating the PAR2/IL-6/JAK1/STAT3 axis through MBD3 degradation, leading to PD-L1 upregulation, which may help develop new therapeutic strategies targeting PD-L1 to improve the efficacy of SBRT in HCC.

Transwell, CCK-8, clone formation, and in vivo tumorigenesis experiments confirmed MBD3's impact on migration, invasion, and proliferation. Our findings demonstrate MBD3 as a potential prognostic marker and therapeutic target for colon cancer.