Overexpression of absent in melanoma 2 in oral squamous cell carcinoma contributes to tumor progression

被引:20
作者
Nakamura, Yuri [1 ,2 ]
Nakahata, Shingo [1 ]
Kondo, Yuudai [2 ]
Izumi, Aya [2 ,3 ]
Yamamoto, Koji [3 ]
Ichikawa, Tomonaga [1 ]
Tamura, Tomohiro [2 ]
Noumi, Kenta [2 ]
Yamashita, Yoshihiro [2 ]
Morishita, Kazuhiro [1 ]
机构
[1] Univ Miyazaki, Div Tumor & Cellular Biochem, Dept Med Sci, Miyazaki, Japan
[2] Univ Miyazaki, Div Oral & Maxillofacial Surg, Dept Med Sensory & Motor Organs, Fac Med, Miyazaki, Japan
[3] Univ Miyazaki, Div Oncopathol & Regenerat Biol, Dept Pathol, Fac Med, Miyazaki, Japan
基金
日本学术振兴会;
关键词
Absent in melanoma 2 (AIM2); Oral squamous cell carcinoma (OSCC); Invasion; Epithelial-mesenchymal transition (EMT); AIM2; INFLAMMASOME; SENSOR; TUMORIGENESIS; CANCER; IFI16;
D O I
10.1016/j.bbrc.2018.12.066
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We had previously reported that in addition to p53 inactivation, overexpression of the DNA sensor protein-absent in melanoma 2 (AIM2)-contributes to tumorigenesis of oral squamous cell carcinoma (OSCC). Given that AIM2 is highly expressed in the OSCC tumors from patients with metastasis, we investigated whether AIM2 expression contributes to the progression of OSCC metastasis. In in vitro assays using OSCC cell lines, the high migration and invasion capacity of OSCC cells were dependent on the increased expression of AIM2, resulting in enhanced epithelial-mesenchymal transition (EMT), with EMT-related gene expression. Moreover, the in vivo short-term metastasis assay using orthotopic implantation into immunodeficient mice demonstrated that OSCC cells with high levels of AIM2 expression exhibited enhanced tumor growth in the tongue, resulting in decreased survival of the mice. Further, the cells overexpressing AIM2 dominantly invaded into the tumor lymphatic vessels, unlike OSCC cells with low AIM2 expression. Thus, the high expression of AIM2 in OSCC enhances progression of tumor growth. (C) 2018 Elsevier Inc. All rights reserved.
引用
收藏
页码:82 / 88
页数:7
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