De Andrea Marco, Gioia Daniela, Mondini Michele, Azzimonti Barbara, Renò Filippo, Pecorari Giancarlo, Landolfo Vincenzo, Tommasino Massimo, Accardi Rosita, Herold-Mende Christel, Landolfo Santo, Gariglio Marisa
Department of Public Health and Microbiology, Medical School of Torino, Via Santena 9, 10126 Torino, Italy.
Head Neck. 2007 Sep;29(9):835-44. doi: 10.1002/hed.20611.
In a previous analysis of head and neck squamous cell carcinomas (HNSCCs), we showed that the levels of the interferon-inducible protein IFI16 inversely correlate with cancer grade. In this study, we further evaluate the molecular role of IFI16 in the development of HNSCCs.
The effect of IFI16 expression was evaluated by its retroviral restoration in an IFI16-negative HNSCC-derived cell line, HNO136. Growth rate and soft agar colony formation were evaluated. The effect of IFI16 restoration in cells exposed to doxorubicin was also analyzed.
IFI16 restoration resulted in the inhibition of both cell growth and in vitro transforming activity and increased doxorubicin-induced cell death by accumulating the cells at the G2/M phase.
In agreement with our previous in vivo data, IFI16 appears to be involved in maintaining the normal growth of epithelial cells, whereas its downregulation may contribute to uncontrolled cell proliferation and tumorigenesis.
在先前对头颈部鳞状细胞癌（HNSCCs）的分析中，我们发现干扰素诱导蛋白IFI16的水平与癌症分级呈负相关。在本研究中，我们进一步评估IFI16在HNSCCs发生发展中的分子作用。
通过在IFI16阴性的HNSCC衍生细胞系HNO136中进行逆转录病毒恢复来评估IFI16表达的影响。评估细胞生长速率和软琼脂集落形成。还分析了IFI16恢复对暴露于阿霉素的细胞的影响。
IFI16恢复导致细胞生长和体外转化活性受到抑制，并通过使细胞停滞在G2/M期增加阿霉素诱导的细胞死亡。
与我们先前的体内数据一致，IFI16似乎参与维持上皮细胞的正常生长，而其下调可能导致细胞增殖失控和肿瘤发生。
