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HIST1H2BN induced cell proliferation and EMT phenotype in prostate cancer via NF-κB signal pathway
Juan Zhang1, Yuhan Chang1, Haiyan Xia2
1Department of Oncology, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China.
Background:
The potential role of HIST1H2BN in prostate cancer remains unclear.
Objective:
To evaluate the carcinogenic role of HIST1H2BN in prostate cancer.
Methods:
The expression of HIST1H2BN in prostate cancer was analyzed using TCGA database and clinical samples. The roles and mechanisms of HIST1H2BN were investigated in DU145 and PC3 cells.
Results:
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.
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