ArticleBioengineered2022
MicroRNA-1269 is downregulated in glioblastoma and its maturation is regulated by long non-coding RNA SLC16A1 Antisense RNA 1.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 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
5 citing papers in PubMed, 5 citations in OpenAlex.
- [Effect of LncRNA DANCR on the immune microenvironment of glioma cells by regulating the miR-656/BMPR1A axis].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026Article
- EP300 regulates the SLC16A1-AS1-AS1/TCF3 axis to promote lung cancer malignancies through the Wnt signaling pathway.Heliyon · 2024Article
- Biological roles of SLC16A1-AS1 lncRNA and its clinical impacts in tumors.Cancer cell international · 2024Review
- The Pivotal Function of SLC16A1 and SLC16A1-AS1 in Cancer Progress: Molecular Pathogenesis and Prognosis.Mini reviews in medicinal chemistry · 2024Article
- HOXC Cluster Antisense RNA 3, a Novel Long Non-Coding RNA as an Oncological Biomarker and Therapeutic Target in Human Malignancies.OncoTargets and therapy · 2023Review
Corrections and comments
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA-1269 (miR-1296) promotes esophageal cancer. However, its role in other cancers, such as glioblastoma (GBM) is unclear. We predicted that miR-1269 might interact with long non-coding RNA (lncRNA) SLC16A1 Antisense RNA 1 (SLC16A1-AS1), a critical player in GBM. We then studied the interaction between SLC16A1-AS1 and miR-1269 in GBM. In this study, paired GBM and non-tumor tissues were used to analyze the expression of SLC16A1-AS1 and premature and mature miR-1269. The interaction of SLC16A1-AS1 with premature miR-1269 was analyzed with RNA pull-down assay and dual-luciferase reporter assay. Cellular fractionation assay was applied to determine the subcellular location of SLC16A1-AS1. Overexpression assays were applied to determine the role of SLC16A1-AS1 in miR-1269 maturation. BrdU, Transwell and cell apoptosis assays were performed to analyze the role of SLC16A1-AS1 and miR-1269 in GBM cell proliferation, migration, and invasion. Interestingly, we observed the upregulation of premature miR-1269 and downregulation of mature miR-1269 in GBM. SLC16A1-AS1 was also overexpressed in GBM. The direct interaction of SLC16A1-AS1 with premature miR-1269 was observed. SLC16A1-AS1 suppressed miR-1269 maturation and promoted cell proliferation, migration, and invasion, and inhibited cell apoptosis, while miR-1269 displayed the opposite trend. SLC16A1-AS1 partly reversed the effects of miR-1269 on GBM cell proliferation, movement and apoptosis. Moreover, SLC16A1-AS1 overexpression increased the level of ki-67, CDK4 and Bcl-2 in LN-229 and LN-18 cells. However, miR-1269 could partly reverse the effect of SLC16A-AS1 on protein levels. Overall, miR-1269 is downregulated in GBM and its maturation is regulated by SLC16A1-AS1.
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