lncRNA MFI2-AS1/miR-125a-5p轴上调TRIAP1促进甲状腺癌肿瘤发生。
Upregulation of TRIAP1 by the lncRNA MFI2-AS1/miR-125a-5p Axis Promotes Thyroid Cancer Tumorigenesis.
作者信息
Yu Tianyu, Tong Lingling, Ao Yu, Zhang Genmao, Liu Yunpeng, Zhang Hejia
机构信息
Department of Thyroid Surgery, Jilin University China-Japan Union Hospital, Changchun 130033, People's Republic of China.
Department of Gynaecology and Obstetrics, Jilin University China-Japan Union Hospital, Changchun 130033, People's Republic of China.
出版信息
Onco Targets Ther. 2020 Jul 17;13:6967-6974. doi: 10.2147/OTT.S236476. eCollection 2020.
BACKGROUND
Thyroid cancer is a very common endocrine cancer worldwide. How long noncoding RNA (lncRNA) regulates thyroid cancer is elusive. LncRNA MFI2-AS1 has been demonstrated to initiate colorectal cancer. Nevertheless, the role of MFI2-AS1 in thyroid cancer remains unknown. This study aims to determine the roles of MFI2-AS1 in thyroid cancer.
METHODS
qRT-PCR was used to determine the expression of MFI2-AS1 in thyroid cancer tissues and cells. Proliferation was determined by using CCK8 and colony formation assays. Transwell assay was utilized to analyze migration and invasion. Luciferase reporter assay was performed to confirm the interaction between MFI2-AS1 and miR-125a-5p.
RESULTS
MFI2-AS1 was shown to be highly expressed in thyroid cancer tissues and predicted poor prognosis. Knockdown of MFI2-AS1 inhibited proliferation, colony formation, migration and invasion of thyroid cancer cells in vitro. Bioinformatics screening identified MFI2-AS1 as the sponge for miR-125a-5p. And miR-125a-5p was further confirmed to target TRIAP1 directly. Our data further demonstrated that MFI2-AS1 promoted TRIAP1 expression via repressing miR-125a-5p. Finally, TRIAP1 was found to be upregulated in thyroid cancer tissues and its restoration reversed the effects of MFI2-AS1 depletion.
CONCLUSION
Our results elucidated a novel mechanism that MFI2-AS1 promotes thyroid cancer progression via the miR-125a-5p/TRIAP1 pathway.
背景
甲状腺癌是全球范围内一种非常常见的内分泌癌。长链非编码RNA（lncRNA）如何调控甲状腺癌尚不清楚。已有研究表明lncRNA MFI2-AS1可引发结直肠癌。然而，MFI2-AS1在甲状腺癌中的作用仍不清楚。本研究旨在确定MFI2-AS1在甲状腺癌中的作用。
方法
采用qRT-PCR检测甲状腺癌组织和细胞中MFI2-AS1的表达。通过CCK8和集落形成试验检测细胞增殖。利用Transwell试验分析细胞迁移和侵袭能力。进行荧光素酶报告基因试验以证实MFI2-AS1与miR-125a-5p之间的相互作用。
结果
MFI2-AS1在甲状腺癌组织中高表达，且提示预后不良。敲低MFI2-AS1可抑制甲状腺癌细胞在体外的增殖、集落形成、迁移和侵袭。生物信息学筛选确定MFI2-AS1为miR-125a-5p的海绵吸附分子。进一步证实miR-125a-5p可直接靶向TRIAP1。我们的数据进一步表明，MFI2-AS1通过抑制miR-125a-5p促进TRIAP1表达。最后，发现TRIAP1在甲状腺癌组织中上调，其恢复表达可逆转MFI2-AS1缺失的影响。
结论
我们的研究结果阐明了一种新的机制，即MFI2-AS1通过miR-125a-5p/TRIAP1途径促进甲状腺癌进展。
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