ArticleArchives of medical science : AMS2020
MiR-376c-3p targets heparin-binding EGF-like growth factor (HBEGF) to inhibit proliferation and invasion in medullary thyroid carcinoma cells.
Article in Archives of medical science : AMS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Methylation-mediated regulation of tumor-suppressor function of the miR-379/656 (C14MC) cluster and its clinical utility in hepatocellular carcinoma.BMC cancer · 2026Article
- Topical Application of Cell-Penetrating Peptide Modified Anti-VEGF Drug Alleviated Choroidal Neovascularization in Mice.International journal of nanomedicine · 2024Article
- Immunological effects of anti-coagulant unfractionated heparin in pregnant Chinese women with cryptic recurrent miscarriages.Archives of medical science : AMS · 2023Article
- microRNA-194 is increased in polycystic ovary syndrome granulosa cell and induce KGN cells apoptosis by direct targeting heparin-binding EGF-like growth factor.Reproductive biology and endocrinology : RB&E · 2021Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAggressive medullary thyroid carcinomas (MTC) have a high mortality rate and the treatment for patients diagnosed with advanced MTC is comparatively ineffective. We hence aimed to test the effects of miR-376c-3p on MTC and to explore the relevant mechanism. MATERIAL AND
methodsCell Counting Kit-8 (CCK-8) and soft agar colony formation assay were applied to evaluate the proliferation of transfected MZ-CRC-1 cells. Wound healing and transwell assay were employed to evaluate MTC cell migration and invasion, respectively. Luciferase assay was performed to validate the downstream target of miR-376c-3p in MZ-CRC-1 cells. Quantitative polymerase chain reaction was used to detect mRNA abundance of key genes. Western blot technique was used to analyze protein levels of HBEGF, E-cadherin, ZO-1, N-cadherin and vimentin.
resultsMiR-376c-3p inhibited the viability, migration and invasion of MZ-CRC-1 cells. Moreover, miR-376c-3p mimic downregulated expression of N-cadherin and vimentin but upregulated that of E-cadherin and ZO-1 in MZ-CRC-1 cells. Results for the luciferase reporter assay showed that miR-376c-3p was able to bind the 3' untranslated region of heparin-binding EGF-like growth factor (HBEGF), of which overexpression nearly nullified the miR-376c-3p mimic-induced inhibitory effects in the MTC cells.
conclusionsMiR-376c-3p showed suppressive effects on MZ-CRC-1 cells via targeting and downregulating HBEGF, suggesting that miR-376c-3p could potentially be targeted for the treatment of MTC.
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