Song Min, Wang Na, Li Zhen, Zhang Yanfang, Zheng Yingying, Yi Pengfei, Chen Jing
Department of Endocrinology, Affiliated Hospital of Jining Medical University, Jining, Shandong, China.
Department of Chest Surgery, Affiliated Hospital of Jining Medical University, Jining, Shandong, China.
J Cell Biochem. 2020 Feb;121(2):984-995. doi: 10.1002/jcb.29333. Epub 2019 Sep 6.
The dysregulation of miR-125a-3p has been observed in multiple tumor types. Nevertheless, the function of miR-125a-3p in papillary thyroid carcinoma (PTC) is yet to be explored. Herein, we find that miR-125a-3p is markedly downregulated in PTC tissues, and its level is inversely related to the histological grade of PTC. Upregulation of miR-125a-3p suppresses the pulmonary metastatic ability as well as the tumor growth of PTC cell in vivo. Consistently, the colony formation ability and other metastasis-related traits of PTC cell are inhibited by miR-125a-3p transfection in vitro. In addition, we identify that matrix metalloprotease 11 (MMP11) is the direct target gene of miR-125a-3p, and that miR-125a-3p inhibits cell viability, migration, and invasiveness of PTC cell by reducing MMP11 expression in vitro. Together, these data testify that the miR-125a-3p/MMP11 axis plays vital roles in the growth and progression of human PTC cells.
在多种肿瘤类型中均观察到miR-125a-3p的失调。然而，miR-125a-3p在甲状腺乳头状癌（PTC）中的功能尚待探索。在此，我们发现miR-125a-3p在PTC组织中显著下调，其水平与PTC的组织学分级呈负相关。miR-125a-3p的上调抑制了PTC细胞在体内的肺转移能力以及肿瘤生长。同样，体外转染miR-125a-3p可抑制PTC细胞的集落形成能力及其他与转移相关的特性。此外，我们确定基质金属蛋白酶11（MMP11）是miR-125a-3p的直接靶基因，并且miR-125a-3p通过在体外降低MMP11的表达来抑制PTC细胞的活力、迁移和侵袭性。总之，这些数据证明miR-125a-3p/MMP11轴在人类PTC细胞的生长和进展中起着至关重要的作用。
