DNA methylation-mediated silencing enhances signaling: implications for asthma pathogenesis.

BACKGROUND

Fibroblast growth factor receptor 1 () is known to play a crucial role in the pathogenesis of asthma, although the precise mechanism remains unclear. This study aims to investigate how DNA methylation-mediated silencing of contributes to the enhancement of NF-κB signaling, thereby influencing the progression of asthma.

METHODS

RT-qPCR was utilized to assess mRNA levels in the serum of asthma patients and BEAS-2B, HBEpiC, and PCS-301-011 cells. CCK8 assays were conducted to evaluate the impact of overexpression on the proliferation of BEAS-2B, PCS-301-011, and HBEpiC cells. Dual-luciferase and DNA methylation inhibition assays were performed to elucidate the underlying mechanism of gene in asthma. The MassARRAY technique was employed to measure the methylation levels of the DNA.

RESULTS

Elevated mRNA levels were observed in the serum of asthma patients compared to healthy controls. Overexpression of in BEAS-2B cells significantly enhanced cell proliferation and stimulated NF-ĸB transcriptional activity in HERK-293T cells. Furthermore, treatment with 5-Aza-CdR, a DNA demethylating agent, markedly increased the expression of mRNA in BEAS-2B, PCS-301-011, and HBEpiC cells. Luciferase activity analysis confirmed heightened NF-ĸB transcriptional activity in -overexpressing BEAS-2B cells and BEAS-2B cells treated with 5-Aza-CdR. Additionally, a decrease in methylation levels in the DNA promoter was detected in the serum of asthma patients using the MassARRAY technique.

CONCLUSION

Our findings reveal a potential mechanism involving in the progression of asthma. DNA methylation of inactivates the NF-ĸB signaling pathway, suggesting a promising avenue for developing effective therapeutic strategies for asthma.