ArticleOncoTargets and therapy2019
Long Non-Coding RNA TUG1 Modulates Proliferation, Migration, And Invasion Of Acute Myeloid Leukemia Cells Via Regulating miR-370-3p/MAPK1/ERK.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 30 citations in OpenAlex.
- Liquid Biopsy in Hematologic Malignancies: Advances, Challenges, and Future Directions.Asia-Pacific journal of clinical oncology · 2026Review
- Long non-coding RNAs in B-cell acute lymphoblastic leukemia: Disease implication, challenges and therapeutic opportunities.Non-coding RNA research · 2026Review
- The potential role of BM-MSC-derived exosomes in TUG1 modulation: antileukemic effects on THP-1 cells.Medical oncology (Northwood, London, England) · 2025Article
- Immune checkpoints and ncRNAs: pioneering immunotherapy approaches for hematological malignancies.Cancer cell international · 2024Review
- The Role of Circular RNA in the Pathogenesis of Chemotherapy-Induced Cardiotoxicity in Cancer Patients: Focus on the Pathogenesis and Future Perspective.Cardiovascular toxicology · 2024Review
- The Role of Long Noncoding RNAs in Progression of Leukemia: Based on Chromosomal Location.MicroRNA (Shariqah, United Arab Emirates) · 2024Review
- LncRNA-Top: Controlled deep learning approaches for lncRNA gene regulatory relationship annotations across different platforms.iScience · 2023Article
- Recent findings on miR‑370 expression, regulation and functions in cancer (Review).Oncology reports · 2023Review
- The Promising Role of Non-Coding RNAs as Biomarkers and Therapeutic Targets for Leukemia.Genes · 2023Review
- Revealing key lncRNAs in cytogenetically normal acute myeloid leukemia by reconstruction of the lncRNA-miRNA-mRNA network.Scientific reports · 2022Article
- Identification of lncRNAs associated with the progression of acute lymphoblastic leukemia using a competing endogenous RNAs network.Oncology research · 2022Article
- NCP-BiRW: A Hybrid Approach for Predicting Long Noncoding RNA-Disease Associations by Network Consistency Projection and Bi-Random Walk.Frontiers in genetics · 2022Article
- Role of long noncoding RNA taurine-upregulated gene 1 in cancers.Molecular medicine (Cambridge, Mass.) · 2021Review
- lncRNA RAET1K Promotes the Progression of Acute Myeloid Leukemia by Targeting miR-503-5p/INPP4B Axis.OncoTargets and therapy · 2021Article
- Emerging crosstalk between long non-coding RNAs and Nrf2 signaling.Cancer letters · 2020Article
- Cell Differentiation Agent-2 (CDA-2) Inhibits the Growth and Migration of Saos-2 Cells via miR-124/MAPK1.Cancer management and research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long non-coding RNA taurine-upregulated gene 1 (lncRNA TUG1) has been discovered to participate in multiple cancers including AML. However, the detailed mechanism of TUG1 in AML remains obscure. MATERIALS AND
methodsAML cell lines HL-60 and Kasumi-1 were taken as cell models. TUG1 knockdown or overexpression cell lines were generated. Then, the biological influence of TUG1 on cancer cells was studied using CCK-8 assay, transwell assay and Western blot in vitro. Interaction between TUG1 and miR-370-3p was determined by bioinformatics analysis, RT-PCR, and luciferase assay. Western blot, RT-PCR, and luciferase assay were carried out to validate the interaction between miR-370-3p and its target gene Mitogen-Activated Protein Kinase 1 (MAPK1).
resultsKnockdown of TUG1 markedly reduced viability and metastasis of AML cells, while its overexpression had the opposite effect. MAPK1 was verified as a target gene of miR-370-3p. TUG1 could reduce the level of functional miR-370-3p, facilitate MAPK1 expression, and in turn activate ERK1/2 signaling.
conclusionTUG1 could modulate malignant phenotypes of AML cells via miR-370-3p/MAPK1/ERK signaling. Our study would help to clarify the mechanism of AML tumorigenesis and progression.
Indexed as
Identifiers
What 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.