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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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Detalles Bibliográficos
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
Descripción
Sumario: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.