Department of Oral Pathology, Hospital of Stomatology, The First Affiliated Hospital, Harbin Medical University, Harbin, 150001, People's Republic of China.
Institute of oral biomedicine, Heilongjiang Academy of Medical Science, Harbin, 150086, People's Republic of China.
Sci Rep. 2021 Oct 1;11(1):19593. doi: 10.1038/s41598-021-99157-4.
IFIX, a newly discovered member of the interferon-inducible HIN-200 family, has been identified as a tumor suppressor in breast cancer; however, the involvement of IFIX in oral cancer are poorly understood. Here, we demonstrate a relationship between the level of IFIX expression and the invasive or migratory abilities of oral squamous cell carcinoma. Higher IFIX expression significantly correlated with clinicopathological parameters such as the histopathological grade of clinical samples. In vitro, IFIX overexpression suppressed the invasiveness of human tongue squamous cell carcinoma CAL-27 cells, and this inhibitory effect was mediated by stabilization of the cytoskeleton through various cytokeratins along with downregulation of paxillin, an intracellular adaptor protein that promotes tumor invasion. This inhibitory effect does not appear to affect the transformation of cancer stem-like cells in this cell culture model. Altogether, these data provide novel insights into the tumor-suppressive function of IFIX, namely, stabilization of the cancer cell cytoskeleton.
IFIX 是干扰素诱导的 HIN-200 家族的新发现成员，已被鉴定为乳腺癌中的肿瘤抑制因子；然而，IFIX 参与口腔癌的机制尚不清楚。在这里，我们证明了 IFIX 表达水平与口腔鳞状细胞癌的侵袭和迁移能力之间存在关系。IFIX 表达水平较高与临床样本的组织病理学分级等临床病理参数显著相关。在体外，IFIX 的过表达抑制了人舌鳞状细胞癌 CAL-27 细胞的侵袭性，这种抑制作用是通过各种细胞角蛋白稳定细胞骨架介导的，同时下调了细胞内衔接蛋白 paxillin，paxillin 促进肿瘤侵袭。这种抑制作用似乎不会影响该细胞培养模型中癌症干细胞样细胞的转化。总的来说，这些数据为 IFIX 的肿瘤抑制功能提供了新的见解，即稳定癌细胞骨架。
