ArticleEndocrine2017
The roles of microRNA-34b-5p in angiogenesis of thyroid carcinoma.
Article in Endocrine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Role of microRNA-34b-5p in cancer and injury: how does it work?Cancer cell international · 2022Review
- Prognostic impact of miR-34b/c DNA methylation, gene expression, and promoter polymorphism in HPV-negative oral squamous cell carcinomas.Scientific reports · 2022Article
- miR-34b-5p promotes renal cell inflammation and apoptosis by inhibiting aquaporin-2 in sepsis-induced acute kidney injury.Renal failure · 2021Observational
- Effects of laparoscopic and traditional open surgery on the levels of IL-6, TNF-α, and Gal-3 in patients with thyroid cancer.Gland surgery · 2021Article
- Molecular Pathology of Poorly Differentiated and Anaplastic Thyroid Cancer: What Do Pathologists Need to Know?Endocrine pathology · 2021Review
- Anaplastic Thyroid Carcinoma: Current Issues in Genomics and Therapeutics.Current oncology reports · 2021Review
- lncRNA-ZFAS1 promotes the progression of endometrial carcinoma by targeting miR-34b to regulate VEGFA expression.Open medicine (Warsaw, Poland) · 2021Article
- Development and validation of a four-microRNA signature for placenta accreta spectrum: an integrated competing endogenous RNA network analysis.Annals of translational medicine · 2020Article
- LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis.Cancer cell international · 2020Article
- Mechanisms of Cardiovascular Disorders in Patients With Chronic Kidney Disease: A Process Related to Accelerated Senescence.Frontiers in cell and developmental biology · 2020Review
- Aberration methylation of miR-34b was involved in regulating vascular calcification by targeting Notch1.Aging · 2019Article
- Article
- Autotaxin exacerbates tumor progression by enhancing MEK1 and overriding the function of miR-489-3p.Cancer letters · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThis study aims to determine the expression of miR-34b-5p in thyroid carcinomas and to investigate the role of miR34b-5p in the modulation of proteins involved in angiogenesis of thyroid carcinoma cells.
methodsThe expressions of miR-34b-5p levels in five cell lines and 65 tissue samples from thyroid carcinomas were examined by real-time polymerase chain reaction. An exogenous miR-34b-5p (mimic) transiently overexpress miR-34b-5p in theses thyroid carcinoma cells. The effects of miR-34b-5p overexpression on the proteins involved in angiogenesis and cell cycle regulations (VEGF-A, Bcl-2 and Notch1) were investigated by Western blot, immunofluorescence, enzyme-linked immunosorbent assay followed by cell cycle analysis and apoptosis assays.
resultsmiR-34b-5p is markedly downregulated in all thyroid carcinoma cell lines and tissues samples when compared with non-neoplastic immortalised thyroid cell line and non-neoplastic thyroid tissues, respectively. The expression levels of miR-34b were significantly associated with T-stages of thyroid carcinomas (p = 0.042). Downregulation of VEGF-A, Bcl-2 and Notch1 proteins in thyroid carcinoma cells were noted in cells that transiently transfected with miR-34b-5p mimic. In addition, enzyme-linked immunosorbent assay confirmed the decreased expression of VEGF in thyroid carcinoma cells after transfection with miR-34b-5p mimic. Furthermore, miR-34b-5p mimic transfection induces significant accumulation of cells in G0-G1 of the cell cycle by blocking of their entry into the S transitional phase as well as increasing the total apoptosis.
conclusionsmiR-34b-5p functions as a potent regulator of angiogenesis, apoptosis and cell proliferation via modulation of VEGF-A, Bcl-2 and Notch1 proteins. It could be a target for developing treatment strategies of thyroid carcinoma with aggressive clinical behaviour.
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