ArticleAmerican journal of translational research2021
LncRNA MIAT promotes the proliferation, migration, and invasion of melanoma cells through recruiting TCF12 and activating NFAT5.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- The Prognostic Value of lncRNA MCM3AP-AS1 on Clinical Outcomes in Various Cancers: A Meta- and Bioinformatics Analysis.Disease markers · 2022Pooled it
- MIAT: A pivotal oncogenic long noncoding RNA tunning the hallmarks of solid malignancies.Translational oncology · 2025Article
- Role of Extracellular Vesicles in TSC Renal Cystogenesis.International journal of molecular sciences · 2025Article
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Article
- LINC00662 promotes melanoma progression by competitively binding miR-107 and activating the β-catenin signaling pathway.International journal of medical sciences · 2024Article
- RNA-binding protein DHX9 promotes glioma growth and tumor-associated macrophages infiltration via TCF12.CNS neuroscience & therapeutics · 2023Article
- The expression level of chicken telomerase reverse transcriptase in tumors induced by ALV-J is positively correlated with methylation and mutation of its promoter region.Veterinary research · 2022Article
- The role of lncRNAs in the tumor microenvironment and immunotherapy of melanoma.Frontiers in immunology · 2022Review
- A novel necroptosis-related lncRNA signature predicts the prognosis and immune microenvironment of hepatocellular carcinoma.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to explore the biological functions and mechanism of long non-coding RNA myocardial infarction-associated transcript (MIAT) in melanoma progression. MIAT expression in melanoma tissue samples and cells was detected by quantitative real-time PCR. After gain-of-function and loss-of-function models were constructed, cell counting kit-8, EdU, and Transwell assays were employed to detect the proliferation, migration, and invasion of melanoma cells. catRAPID database was employed and RNA pull-down assay and RNA immunoprecipitation assay were utilized to verify, the binding relationship between MIAT and transcription factor 12 (TCF12). The binding of TCF12 to the promoter region of the gene of nuclear factor of activated T cells 5 (NFAT5) was verified by chromatin immunoprecipitation-quantitative PCR assay and dual-luciferase reporter gene assay. The regulatory effects of MIAT and TCF12 on NFAT5 expression were detected via Western blot. The results showed that MIAT expression was increased in melanoma tissues and cells, and was significantly associated with the AJCC stage and the differentiation of melanoma tissues. MIAT overexpression markedly facilitated melanoma cells' multiplication, migration, and invasion, while MIAT knockdown inhibited the multiplication, migration, and invasion. MIAT showed direct interaction with TCF12. MIAT promoted the binding of TCF12 to NFAT5 promoter region, thereby promoting NFAT5 transcription. In conclusion, MIAT promotes melanoma progression through recruiting TCF12 and its interaction with NFAT5.
Indexed as
Identifiers
34956475PMC8661192W4206892772What OpenQuestion holds
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.