MicroRNA-221 promotes papillary thyroid carcinoma cells migration and invasion via targeting RECK and regulating epithelial–mesenchymal transition
Authors Wei Z, Gao A, Wang Q, Lou X, Zhao J, Lu Q
Received 10 October 2018
Accepted for publication 6 February 2019
Published 28 March 2019 Volume 2019:12 Pages 2323—2333
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Cristina Weinberg
Peer reviewer comments 4
Editor who approved publication: Dr XuYu Yang
Zhao-li Wei,1 Ai-bin Gao,1 Qing Wang,1 Xiu-e Lou,1 Jing Zhao,2 Qing-jun Lu3
1Department of Endocrinology, Binzhou Central Hospital, Binzhou Medical University, Binzhou 251700, Shandong Province, People’s Republic of China; 2Department of Oncology, Provincal Hospital of Shandong University, Jinan 250000, Shandong Province, People’s Republic of China; 3Department of Oncology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200001, People’s Republic of China
Aim: The aim of this study was to detect the effects and potential mechanisms of microRNA-221 on a series of biological behaviors of papillary thyroid carcinoma (PTC) cells in vitro and in vivo.
Methods: First, we analyzed the relationship between the expression of miR-221 and several clinicopathological features of PTC patients and then detected the expression of the miR-221 in tumor tissues and cell lines. The effects of miR-221 on proliferation and invasion of PTC cells were verified by cell counting kit-8 (CCK-8) assay, wound healing assay and transwell assay. Western blot assay was applied to explore the correlation between miR-221 and RECK expression in PTC K1 cells. Finally, a xenograft model was established to further confirm the tumor-promoting effects of miR-221 in vivo.
Results: Our data indicated that miR-221 was relatively upregulated in metastatic PTC tissues. MiR-221 promoted the proliferation, migration and invasion activities of PTC K1 cells, following variations of epithelial–mesenchymal transition (EMT)-related protein expression. We identified RECK as a direct target of miR-221, revealed its expression to be inversely correlated with miR-221 in PTC samples and showed that its reintroduction reverses miR-221-induced PTC invasiveness. In addition, miR-221 was also verified to promote tumor growth and increase tumor volume and weight in vivo. Taken together, miR-221/RECK axis could be an effective way to regulate biological behaviors of PTC.
Conclusion: MiR-221 may be involved in PTC cell invasion and metastasis by targeting RECK, indicating that the miR-221/RECK pathway could be studied further as a potential new diagnostic or prognostic biomarker for PTC.
Keywords: miR-221, papillary thyroid carcinoma, invasion, RECK
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