ArticleOpen medicine (Warsaw, Poland)2019
Expression and Role of MicroRNA-663b in Childhood Acute Lymphocytic Leukemia and its Mechanism.
Article in Open medicine (Warsaw, Poland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
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- Integrative Analysis of miRNA and mRNA Expression Profiles in Mammary Glands of Holstein Cows Artificially Infected withPathogens (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have shown that microRNAs (miRNAs) play a key role in various malignant tumors. MiR-663b has been found to have important roles in several cancers, however, the role of miR-663b in T cell acute lymphocytic leukemia (T-ALL) remains unclear. Therefore, we speculated that miR-663b might also play a crucial role in the development and process of T-ALL. In the present study, we found that miR-663b was up-regulated in the blood of children with T-ALL and T-ALL cell lines. TargetScan and dual luciferase reporter assay results showed that CD99 was a direct target of miR-663b. In order to further study the biological function of miR-663b in the development of T-ALL and to clarify its potential molecular mechanism, we detected the changes in proliferation, apoptosis, migration, and invasion of T-ALL cell line Jurkat before and after miR-663b inhibitor transfection. We found that miR-663b inhibitor inhibited Jurkat cell proliferation and induced apoptosis. In addition, miR-663b inhibitor repressed Jurkat cell migration and invasion. All these effects of miR-663b inhibitor on Jurkat cells were eliminated by CD99-silencing. These results have provided a new theoretical basis and strategy for the diagnosis and treatment of T-ALL.
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Registered trials
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