ArticleArchives of medical science : AMS2023
MicroRNA-575 targets Derlin 1 to regulate proliferation, migration and invasion of human thyroid cancer cells.
Article in Archives of medical science : AMS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Silencing circRNA-ZFAND6 induces trophoblast apoptosis by activating the mitochondrial pathway through the miR-575/SOD2 axis in unexplained recurrent spontaneous abortion.BMC women's health · 2025Article
- Urinary microRNA-210-3p as a novel and non-invasive biomarker for the detection of pancreatic cancer, including intraductal papillary mucinous carcinoma.BMC cancer · 2024Article
- Identification of differentially expressed ER stress-related genes and their association with pulmonary arterial hypertension.Respiratory research · 2024Article
- MiR-575 in Exosomes of Vaginal Discharge Is Downregulated in Ovarian Cancer Patients.Cancer genomics & proteomicsArticle
- Knockdown of Derlin-1 Represses Cellular Oncogenic Activities in Uveal Melanoma, Enhances its Chemosensitivity to Cisplatin and Reduces Cancer Stem Cell Potential.Cancer genomics & proteomicsArticle
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Authors and funding
5 authors.
Funding
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Abstract
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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