Therefore, we propose that SFN and ECN may inhibit bladder carcinogenesis via epigenetic modulation of gene expression associated with histone H1 phosphorylation.
In the present study, we showed that HMGN5, a nucleosome binding protein that can unfold chromatin by binding to histone (H1), is overexpressed in prostate cancer cells and plays an oncogenic role in prostate cancer tumorigenesis and development by activating the MAPK signaling pathway.
Changes in histone H1 phosphorylation status may further clarify epigenetic changes during bladder carcinogenesis and provide diagnostic and prognostic biomarkers or targets for future therapeutic interventions.