Article Sidebar
Published:
Jan 12, 2022DOI:
10.4314/tjpr.v20i2.5Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
MiR-557 downregulation lowered cell proliferation and malignancy in glioblastoma by targeting ADAM17
Abstract
Purpose: To examine the role of miR-557 in the pathogenesis and development of glioblastoma (GBM) and its potential regulatory mechanism.
Methods: Dysregulation of miR-557 in GBM cells was determined using quantitative (real-time) PCR (qPCR). Cell proliferative ability, migratory activity and invasive ability were measured using the MTT colorimetric assay, wound healing assay and Transwell chambers assay. The direct target mRNA of miR-557 was predicted, and further validated using TargetScan and luciferase assay, respectively.
Results: Compared with human astrocytes (HAs), the downregulation of miR-557 was observed in human GBM cell lines. In U-251MG and A172 cells that overexpressed miR-557 mimics, the level of proliferation was significantly reduced, the wound width was larger, and the number of invaded cells wan decreased than that of NC mimics. Predictive results from TargetScan and results of luciferase assay demonstrated that miR-557 directly targets the 3’-untranslated region (3’-UTR) of ADAM17. In A172 cells and U-251MG cells, the upregulation E-cadherin (E-cad) and the downregulation of N- cadherin (N-cad) and vimentin (Vim) were caused by miR-557 mimics as compared with NC mimics. Expression of ADAM17, NICD, HES1, and EGFR was downregulated by miR-557 mimics and upregulated by miR-557 inhibitors in A172 cells and U-251MG cells.
Conclusion: Downregulation of miR-557 accelerates GBM cell growth and malignancy by directly targeting ADAM17 3’-UTR, providing a prognostic and potential therapeutic factor for new drug discovery in GBM.
