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MicroRNA-575 targets Derlin 1 to regulate proliferation, migration and invasion of human thyroid cancer cells

INTRODUCTION: This study was undertaken to examine the expression of miR-575 in thyroid cancer tissues and to explore its therapeutic potential. MATERIAL AND METHODS: Expression analysis was carried out by qRT-PCR. The MTT assay was used for cell viability. DAPI and annexin V/PI assays were used to...

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Autores principales: Dong, Hong, Wu, Yan-Le, Zhang, Xin, Li, Han-Lin, Zheng, Wei-Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10408017/
https://www.ncbi.nlm.nih.gov/pubmed/37560720
http://dx.doi.org/10.5114/aoms.2020.92867
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author Dong, Hong
Wu, Yan-Le
Zhang, Xin
Li, Han-Lin
Zheng, Wei-Hong
author_facet Dong, Hong
Wu, Yan-Le
Zhang, Xin
Li, Han-Lin
Zheng, Wei-Hong
author_sort Dong, Hong
collection PubMed
description INTRODUCTION: This study was undertaken to examine the expression of miR-575 in thyroid cancer tissues and to explore its therapeutic potential. MATERIAL AND METHODS: Expression analysis was carried out by qRT-PCR. The MTT assay was used for cell viability. DAPI and annexin V/PI assays were used to detect apoptosis. Wound healing and Transwell assays were used for cell migration and invasion respectively. Western blot analysis was used to determine the expression of proteins. RESULTS: The results showed significant downregulation of miR-575 in thyroid cancer tissues and cell lines. The role of miR-575 was deciphered by overexpression of miR-575 in MDA-T32 and MDA-T68 thyroid cancer cells. The results showed that overexpression of miR-575 caused significant inhibition of the proliferation of the MDA-T32 and MDA-T68 cells via induction of apoptotic cell death. The expression of Bax was also enhanced while that of Bax was decreased upon miR-575 overexpression in MDA-T32 and MDA-T68 cells. Additionally, miR-575 overexpression inhibited the migration and invasion of the MDA-T32 and MDA-T68 thyroid cancer cells. Bioinformatic approaches and the dual luciferase assay indicated Derlin 1 (DERL1) to be the potential target of miR-575 in thyroid cancer. DERL1 was significantly upregulated in thyroid cancer tissues and cell lines and overexpression of miR-575 caused suppression of DERL1 in MDA-T68 cells. Silencing of DERL1 inhibited the proliferation of the MDA-T68 cells while overexpression of DERL1 could abolish the effects of miR-575 overexpression on the proliferation of MDA-T68 thyroid cancer cells. CONCLUSIONS: miR-575 may be used as a therapeutic target for thyroid cancer treatment.
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spelling pubmed-104080172023-08-09 MicroRNA-575 targets Derlin 1 to regulate proliferation, migration and invasion of human thyroid cancer cells Dong, Hong Wu, Yan-Le Zhang, Xin Li, Han-Lin Zheng, Wei-Hong Arch Med Sci Basic Research INTRODUCTION: This study was undertaken to examine the expression of miR-575 in thyroid cancer tissues and to explore its therapeutic potential. MATERIAL AND METHODS: Expression analysis was carried out by qRT-PCR. The MTT assay was used for cell viability. DAPI and annexin V/PI assays were used to detect apoptosis. Wound healing and Transwell assays were used for cell migration and invasion respectively. Western blot analysis was used to determine the expression of proteins. RESULTS: The results showed significant downregulation of miR-575 in thyroid cancer tissues and cell lines. The role of miR-575 was deciphered by overexpression of miR-575 in MDA-T32 and MDA-T68 thyroid cancer cells. The results showed that overexpression of miR-575 caused significant inhibition of the proliferation of the MDA-T32 and MDA-T68 cells via induction of apoptotic cell death. The expression of Bax was also enhanced while that of Bax was decreased upon miR-575 overexpression in MDA-T32 and MDA-T68 cells. Additionally, miR-575 overexpression inhibited the migration and invasion of the MDA-T32 and MDA-T68 thyroid cancer cells. Bioinformatic approaches and the dual luciferase assay indicated Derlin 1 (DERL1) to be the potential target of miR-575 in thyroid cancer. DERL1 was significantly upregulated in thyroid cancer tissues and cell lines and overexpression of miR-575 caused suppression of DERL1 in MDA-T68 cells. Silencing of DERL1 inhibited the proliferation of the MDA-T68 cells while overexpression of DERL1 could abolish the effects of miR-575 overexpression on the proliferation of MDA-T68 thyroid cancer cells. CONCLUSIONS: miR-575 may be used as a therapeutic target for thyroid cancer treatment. Termedia Publishing House 2020-02-04 /pmc/articles/PMC10408017/ /pubmed/37560720 http://dx.doi.org/10.5114/aoms.2020.92867 Text en Copyright: © 2020 Termedia & Banach https://creativecommons.org/licenses/by-nc-sa/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
spellingShingle Basic Research
Dong, Hong
Wu, Yan-Le
Zhang, Xin
Li, Han-Lin
Zheng, Wei-Hong
MicroRNA-575 targets Derlin 1 to regulate proliferation, migration and invasion of human thyroid cancer cells
title MicroRNA-575 targets Derlin 1 to regulate proliferation, migration and invasion of human thyroid cancer cells
title_full MicroRNA-575 targets Derlin 1 to regulate proliferation, migration and invasion of human thyroid cancer cells
title_fullStr MicroRNA-575 targets Derlin 1 to regulate proliferation, migration and invasion of human thyroid cancer cells
title_full_unstemmed MicroRNA-575 targets Derlin 1 to regulate proliferation, migration and invasion of human thyroid cancer cells
title_short MicroRNA-575 targets Derlin 1 to regulate proliferation, migration and invasion of human thyroid cancer cells
title_sort microrna-575 targets derlin 1 to regulate proliferation, migration and invasion of human thyroid cancer cells
topic Basic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10408017/
https://www.ncbi.nlm.nih.gov/pubmed/37560720
http://dx.doi.org/10.5114/aoms.2020.92867
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