HIST1H2BN induced cell proliferation and EMT phenotype in prostate cancer via NF-κB signal pathway.

HIST1H2BN was significantly upregulated in prostate cancer. HIST1H2BN knockdown inhibited cell proliferation, migration and EMT phenotype in prostate cancer cells. Downregulating HIST1H2BN diminished the expression and binding activity of NF-κB p65, then influenced the expression of MMP2 and MMP9. CONCLUSION : This is the first study to elaborate a HIST1H2BN-NF-κB-EMT regulatory axis in oncogenesis, indicating that HIST1H2BN might be potential therapeutic target for prostate cancer.