Although viruses can cause cancer, other studies reported the regression of human tumors upon viral infections. We investigated the cytoreductive potential of human cytomegalovirus (HCMV) in a murine model of human hepatocellular carcinoma (HCC) in severe-immunodeficient mice. Infection of HepG2 cells with HCMV resulted in the absence of tumor or in a limited tumor growth following injection of cells subcutaneously. By contrast all mice injected with uninfected HepG2 cells and with HepG2 cells infected with UV-treated HCMV did develop tumors without any significant restriction. Analysis of tumors indicated that in mice injected with HCMV-infected-HepG2 cells, but not in controls, a restricted cellular proliferation was observed parallel to a limited activation of the STAT3-cyclin D1 axis, decreased formation of colonies in soft agar, and activation of the intrinsic apoptotic pathway. We conclude that HCMV can provide antitumoral effects in a murine model of HCC which requires replicative virus at some stages that results in limitation of tumor cell proliferation and enhanced apoptosis mediated through the intrinsic caspase pathway.

中文翻译：

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人巨细胞病毒在肝细胞癌小鼠模型中的肿瘤控制。

尽管病毒可以引起癌症，但其他研究报道了病毒感染后人类肿瘤的消退。我们调查了人类巨细胞病毒（HCMV）在严重免疫缺陷小鼠的人类肝细胞癌（HCC）小鼠模型中的细胞还原潜力。用HCMV感染HepG2细胞导致无肿瘤或皮下注射细胞后肿瘤生长受限。相比之下，所有注射了未感染的HepG2细胞和被紫外线处理的HCMV感染的HepG2细胞的小鼠都确实发展了肿瘤，而没有任何明显的限制。肿瘤分析表明，在注射了HCMV感染的HepG2细胞的小鼠中，但未在对照组中，观察到细胞增殖受限，与STAT3-cyclin D1轴的激活受限，软琼脂中菌落形成的减少，和内在的凋亡途径的激活。我们得出结论，HCMV可以在需要在某些阶段复制病毒的HCC鼠模型中提供抗肿瘤作用，这会限制肿瘤细胞的增殖并增强通过固有caspase途径介导的凋亡。