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Copyright (c) 2023 Lingjie Zhang, Rui Ge, Aiqun Cheng, Tianhua Hu
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.MiR-1284 suppresses the proliferation and migration of thyroid cancer
Corresponding Author(s) : Lingjie Zhang
Cellular and Molecular Biology,
Vol. 69 No. 8: Issue 8
Abstract
To elucidate the role of microRNA-1284 (miR-1284) in the onset of thyroid cancer (TC) and its underlying mechanism. Differential expressions of miR-1284 in TC and thyroid tissues were detected. Regulatory effects of miR-1284 on proliferative, migratory, apoptotic potentials and cell cycle progression were assessed. In addition, miR-1284 levels in TC tissues and peripheral blood of TC patients were determined as well. Through collecting culture medium and exosomes of PTC cells, changes in miR-1284 levels were examined. MiR-1284 was downregulated in TC than normal thyroid tissues. Overexpression of miR-1284 attenuated proliferative and migratory potentials, but induced apoptosis in TPC-1 and FTC-133 cells. Moreover, overexpression of miR-1284 upregulated E-cadherin and downregulated N-cadherin in papillary TC (PTC) cells. MiR-1284 was downregulated in TC tissues, while its level in the peripheral blood of TC patients was upregulated. Besides, miR-1284 was upregulated in the culture medium and exosomes of PTC cells, which was reversed by Brefeldin A treatment. Overexpression of miR-1284 suppresses proliferative and migratory potentials and induces apoptosis in TC. Upregulated miR-1284 in the peripheral blood of TC patients may be derived from exosomes secreted by PTC cells.
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