Upregulation of TRIAP1 by the lncRNA MFI2-AS1/miR-125a-5p Axis Promotes Thyroid Cancer Tumorigenesis
Authors Yu T, Tong L, Ao Y, Zhang G, Liu Y, Zhang H
Received 29 October 2019
Accepted for publication 16 May 2020
Published 17 July 2020 Volume 2020:13 Pages 6967—6974
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Jianmin Xu
Tianyu Yu,1,* Lingling Tong,2,* Yu Ao,3 Genmao Zhang,4 Yunpeng Liu,5 Hejia Zhang4
1Department of Thyroid Surgery, Jilin University China-Japan Union Hospital, Changchun 130033, People’s Republic of China; 2Department of Gynaecology and Obstetrics, Jilin University China-Japan Union Hospital, Changchun 130033, People’s Republic of China; 3Department of Pediatrics, Jilin University First Hospital, Changchun 130031, People’s Republic of China; 4Department of Ultrasound, Jilin University China-Japan Union Hospital, Changchun 130033, People’s Republic of China; 5Department of Thoracic Surgery, Jilin University First Hospital, Changchun 130031, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Hejia Zhang
Department of Ultrasound, Jilin University China-Japan Union Hospital, Changchun 130033, People’s Republic of China
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.
Keywords: MFI2-AS1, miR-125a-5p, TRIAP1, proliferation, thyroid cancer
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