ArticleOncology letters2017
NLS-RARα is a novel transcriptional factor.
Article in Oncology letters, 2017. 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, 2 citations in OpenAlex.
- Nanocarrier-Based Systems for Targeted Delivery: Current Challenges and Future Directions.MedComm · 2025Review
- NLS‑RARα modulates acute promyelocytic leukemia NB4 cell proliferation and differentiation via the PI3K/AKT pathway.Molecular medicine reports · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute promyelocytic leukemia (APL) is characterized by the presence of the promyelocytic leukemia (PML)-retinoic acid receptor-α (RAR-α) fusion protein. PML-RARα can be cleaved by neutrophil elastase (NE) in several positions in cells in the promyelocytic stage, nuclear location signal (NLS)-negative PML and NLS-RARα may be the products of PML-RARα by NE. The function of NLS-RARα may be affected by the addition of NLS, which would alter its localization in cells, as the role of NLS is to identify proteins for transport to the nucleus. Preliminary experiments demonstrated that the overexpression of NLS-RARα in HL-60 cells could promote cellular proliferation and inhibit cellular differentiation. Following treatment with all-trans retinoic acid (ATRA), the degree of cellular differentiation was enhanced. In the present study, the localization of NLS-RARα was identified and its activity as a novel transcriptional factor was assessed, which may be critical in the development of APL. The location of NLS-RARα was detected in the nucleus and cytoplasm by indirect immunofluorescence and western blot analysis, with expression in the nucleus revealed to be increased compared with that in the cytoplasm. Next, native-PAGE was performed and NLS-RARα and RXRα were revealed to form heterodimers in the nucleus. In addition, co-immunoprecipitation revealed an interaction between NLS-RARα and retinoid X receptor-α (RXRα). An electrophoresis mobility shift assay (EMSA) indicated that NLS-RARα could bind retinoic acid response elements (RAREs) in the presence of ATRA. Indeed, NLS-RARα could bind RAREs just as WTRARα could, including the RAREs direct repeat-2 (DR-2) and DR-5. In addition, results from a luciferase reporter gene assay demonstrated that NLS-RARα could mediate the activity of RAREs that it bound. Together, these results indicated that NLS-RARα may be a novel transcription factor that contributes to leukemogenesis by competitively binding RAREs as heterodimers with RXRα, just as PML-RARα does, thus repressing the gene transcription essential for myeloid differentiation. These findings indicate the potential role of NLS-RARα targeted therapy in APL.
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