ArticleJournal of cellular and molecular medicine2020
MiR-30a-5p inhibits proliferation and metastasis of hydatidiform mole by regulating B3GNT5 through ERK/AKT pathways.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Impacts of β-1, 3-N-acetylglucosaminyltransferases (B3GNTs) in human diseases.Molecular biology reports · 2024Review
- PREDICT-GTN 1: Can we improve the FIGO scoring system in gestational trophoblastic neoplasia?International journal of cancer · 2023Article
- miR-30a targets STOX2 to increase cell proliferation and metastasis in hydatidiform moles via ERK, AKT, and P38 signaling pathways.Cancer cell international · 2022Article
- Circular RNA PUM1 (CircPUM1) attenuates trophoblast cell dysfunction and inflammation in recurrent spontaneous abortion via the MicroRNA-30a-5p (miR-30a-5p)/JUNB axis.Bioengineered · 2021Article
- MiR-30a-5p inhibits proliferation and metastasis of hydatidiform mole by regulating B3GNT5 through ERK/AKT pathways.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hydatidiform moles are gestational trophoblastic disease. They are abnormal proliferations of trophoblast cells that have the potential to become cancerous. miR-miR30a-5p is a tumour suppressor that participates in the development of numerous diseases. However, the role of miR-30a in hydatidiform moles and the mechanisms underlying its effects are presently unclear. This study explored the levels of miR-30a and B3GNT5 expression in human hydatidiform mole tissue. The results showed that miR-30a and B3GNT5 were differentially expressed in normal placenta and hydatidiform mole, and miR-30a decreased cell proliferation, invasion and migration in trophoblast cell lines. Upon further examination, it was confirmed that miR-30a directly targeted the 3'untranslated region of B3GNT5 using a dual-luciferase assay. The results of the present study also revealed that miR-30a reduced the proliferation, invasion and migration ability in JAR and BeWo cells by regulating B3GNT5, which may inactivate the ERK and AKT signalling pathways. This study demonstrated that miR-30a was a novel target B3GNT5 that serves an important role in the development of hydatidiform moles, suggesting that miR-30a may serve as a novel potential biomarker or useful diagnostic and therapeutic tool for hydatidiform moles in clinical settings.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.