ArticleOpen medicine (Warsaw, Poland)2022
Role of lncRNA MIAT/miR-361-3p/CCAR2 in prostate cancer cells.
Article in Open medicine (Warsaw, Poland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- lncRNA MIAT promotes luminal B breast cancer cell proliferation, migration, and invasion in vitro.Journal of applied genetics · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The study was aimed to investigate the role and mechanism of long non-coding RNAs (lncRNA) myocardial infarction-associated transcript (MIAT) in prostate cancer. The relationships between lncRNA MIAT and miR-361-3p, miR-361-3p and cell cycle and apoptosis regulator 2 (CCAR2) were predicted by StarBase and TargetScan, and verified by dual-luciferase reporter assay and RNA pull-down assay. Quantitative real-time PCR assay was performed to detect the mRNA expression of lncRNA MIAT, miR-361-3p, CCAR2, Bax, and Bcl-2 in the prostate cancer tissues or cells. The protein levels of CCAR2, Bax, and Bcl-2 were detected by Western blot analysis. The cell viability and apoptosis were detected by MTT assay and Flow cytometry analysis, respectively. lncRNA MIAT was upregulated, while miR-361 was downregulated in the prostate cancer tissues and Du145 cells. lncRNA MIAT negatively regulated miR-361-3p expression in Du145 cells. Downregulating lncRNA MIAT decreased the cell viability, induced the cell apoptosis, increased Bax expression, and decreased Bcl-2 expression in Du145 cells, while the effects were reversed by downregulating miR-361-3p or CCAR2 upregulation. Moreover, CCAR2 upregulation reversed the effects of miR-361-3p upregulation on Du145 cell viability and apoptosis. In conclusion, lncRNA MIAT participated in prostate cancer by regulating cell proliferation and apoptosis via miR-361-3p/CCAR2 axis.
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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.