科研之友
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摘要
Hepatocellular carcinoma (HCC) accounts for many cases of cancer-associated mortality. Tumor necrosis factor (TNF)-alpha is a key mediator of tumor-promoting inflammation. It has been demonstrated that anti-TNF-alpha treatments have preclinical benefits for multiple types of cancer, however their potential for treating HCC remains unclear. Through fluorescence-activated cell sorter analysis and enzyme-linked immunosorbent assay, the results of the current study indicated that TNF-alpha was strongly expressed in HCC tissues and the HCC cell lines HepG2 and Hep3B. In vitro, anti-TINT-alpha antibodies (infliximab and etanercept) decreased HCC cell viability via antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity effects. Infliximab treatment also significantly increased apoptosis in HepG2 and Hep3B cells compared with controls (P<0.001 and P<0.05, respectively). In vivo, anti-TNF-alpha treatment delayed HCC progression as indicated by the significantly prolonged survival time in an HCC xenograft mouse model (P=0.0009). Further analyses revealed that anti-TNF-alpha treatment significantly decreased the expression of pro-inflammatory cytokines, including TNT-alpha (P<0.01), interleukin (IL)-1 beta (P<0.0.5), IL-6 (P<0.05) and IL-17 (P<0.05) and induced apoptosis in HCC tumors. The results of the current study suggest that TNT-alpha is a potential target for novel therapeutic strategies to treat HCC. Anti-TNF-alpha treatments compromised HCC tumor progression by inducing cell death and decreasing levels of pro-inflammatory cytokines.
- 出版日期2018-8
- 单位潍坊市人民医院; 青岛大学
