ArticleAmerican journal of translational research2019
LncRNA DLX6-AS1 promotes laryngeal squamous cell carcinoma growth and invasion through regulating miR-376c.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Long non-coding RNA DLX6-AS1 is the key mediator of glomerular podocyte injury and albuminuria in diabetic nephropathy by targeting the miR-346/GSK-3β signaling pathway.Cell death & disease · 2023Article
- LncRNA NCK1-AS1 Promotes Malignant Cellular Phenotypes of Laryngeal Squamous Cell Carcinoma via miR-137/NCK1 Axis.Molecular biotechnology · 2022Article
- DLX6-AS1: A Long Non-coding RNA With Oncogenic Features.Frontiers in cell and developmental biology · 2022Review
- Article
- Strategies of LncRNA DLX6-AS1 on Study and Therapeutics.Frontiers in genetics · 2022Review
- Research progress of DLX6-AS1 in human cancers.Human cell · 2021Review
- Article
- ELFN1-AS1 accelerates cell proliferation, invasion and migration via regulating miR-497-3p/CLDN4 axis in ovarian cancer.Bioengineered · 2020Article
- MAGE-A genes as predictors of the outcome of laryngeal squamous cell carcinoma.Oncology letters · 2020Article
- Regulatory Mechanisms of lncRNAs and Their Target Gene Signaling Pathways in Laryngeal Squamous Cell Carcinoma.Frontiers in pharmacology · 2020Review
- Loading MicroRNA-376c in Extracellular Vesicles Inhibits Properties of Non-Small Cell Lung Cancer Cells by Targeting YTHDF1.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence showed that lncRNAs play important roles in tumour development. Recently, a novel lncRNA DLX6-AS1 was found to be overexpressed in some tumors such as lung adenocarcinoma, renal cell carcinoma and hepatocellular carcinoma. However, the functional roles of DLX6-AS1 in laryngeal squamous cell carcinoma (LSCC) are still unclear. In the study, we showed that the expression level of DLX6-AS1 was upregulated in the LSCC samples compared to the noncancerous tissues. By using CCK-8 analysis, we demonstrated that knockdown expression of DLX6-AS1 suppressed the Hep2 cell growth. DLX6-AS1 knockdown inhibited the Hep2 cell cycle and invasion. MiR-376c was identified to have the complementary binding sites with the DLX6-AS1. By luciferase reporter assay, we indicated that overexpression of miR-376c inhibited the luciferase activity of wild-type DLX6-AS1, but it failed to suppress luciferase activity of mutated one. DLX6-AS1 knockdown enhanced the expression of miR-376c in the Hep2 cell. Moreover, we showed that the expression level of miR-376c was lower in the LSCC samples than in the noncancerous tissues and the expression of miR-376c was negatively correlated with expression of DLX6-AS1 in LSCC tissues. Ectopic expression of miR-376c suppressed cell proliferation, cycle and invasion of LSCC cell. DLX6-AS1 knockdown suppressed cell proliferation, cycle and invasion via regulating miR-376c expression. These data proved that lncRNA DLX6-AS1 might play as an oncogene in LSCC development and tumorigenesis.
Indexed as
Identifiers
31814904PMC6895517W3007635929What 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.