ArticleHeliyon2019
RNAi-mediated knockdown of VDR surprisingly suppresses cell growth in Jurkat T and U87-MG cells.
Article in Heliyon, 2019. 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.
- Loss of the vitamin D receptor triggers senescence in chronic myeloid leukemia via DDIT4-mediated DNA damage.Journal of molecular cell biology · 2024Article
- Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vitamin D receptor (VDR) is a nuclear receptor for 1,25-Dihydroxyvitamin D3. VDR is expressed in many types of cells and involved in different biological processes such as immunity and inflammation. In addition, the role for VDR has been indicated in different diseases including multiple sclerosis (MS). In this study, we investigated the effects of VDR knockdown on growth, apoptosis, cell cycle, and some inflammatory gene expressions in Jurkat and U87-MG cell lines. The cell lines were transfected with plasmids encoding short hairpin RNA specific to VDR mRNA. Next, growth, apoptosis, and cell cycle were evaluated using MTT assay and annexin VDR along with flowcytometry. Then the mRNA expression of some genes was determined by real-time PCR at 24 h and 48 h after transfection. The cell growth and apoptosis of VDR-shRNA transfected Jurkat T cells and U87-MG cells were surprisingly changed compared with those in control cells. The expression of IL-10, NF-KB, TGF-β1, TGF-β R I, and TGF-β R II in two cell lines transfected with VDR-shRNA was significantly changed compared to control cells. VDR showed a new unexpected function to control cell growth in vitro. In addition, while VDR knocking down in two different cell lines of U87-MG and Jurkat cells had different effects on NF-kB and TGF-beta expression levels, its effects on cell growth and apoptosis were similar. This may suggest that these two different cell lines can show similar anti-proliferative effects by different downstream signalling pathways. Therefore, these data may be useful to design novel diagnostic and therapeutic methods for diseases such as MS.
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Registered trials
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