Haiyan Xia1, Luwei Xu2, Xiaowei Wei3, Juan Zhang4, Yuhan Chang4. 1. Department of Oncology, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China. haiyxia@njmu.edu.cn. 2. Department of Urinary surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China. xuluwei1980@126.com. 3. Department of Oncology, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China. gswxw@njmu.edu.cn. 4. Department of Oncology, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China.
Abstract
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.
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.