Abstract
In recent years, more and more studies have shown that HBV is closely related to DLBCL and is an important adverse prognostic factor. The purpose of this study was to explore the mechanism of BCL-6 on Hepatitis B Virus (HBV) positive diffuse large B cell lymphoma (DLBCL). In vitro, electrotransfection transfers HBV DNA into the DLBCL cell line; Plasmid was transfected into DLBCL cells to construct hepatitis B virus X protein (HBX) overexpressed DLBCL cells; Cell proliferation was detected by Cell Counting Kit-8;Protein expression was measured by Western blot analysis;Cell apoptosis and cycle analysis were evaluated via flow cytometry. Tumor-bearing mice were used to evaluate antitumor efficacy in vivo. The results showed that HBX increased the expression of BCL-6 gene in DLBCL cell line, promoted the proliferation of DLBCL cell line, induced transformation of cell cycle from G1 phase to S phase, and simultaneously promoted the activation of NF-κB pathway. The upregulation of BCL-6 expression induced by HBX were reversed by BCL-6 inhibitors. In addition, BCL-6 inhibitors inhibited the proliferation of DLBCL cell lines overexpressing HBX by promoting apoptosis. According to these findings, HBX might promote cell proliferation through BCL-6 mediated NF-κB signaling in DLBCL cell lines.
