ArticleMedical science monitor : international medical journal of experimental and clinical research2020
Nicotinamide Inhibits Glycolysis of HL-60 Cells by Modulating Sirtuin 1 (SIRT1)/Peroxisome Proliferator-Activated Receptor γ Coactivator 1α (PGC-1α)/Hypoxia-Inducible Factor-2α (HIF2α) Signaling Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed, 0 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Nicotinamide can affect differentiation and proliferation of leukemia cells. This research aimed to explore the regulatory effect of nicotinamide on glycolysis metabolism of leukemia cells and to clarify the associated mechanisms. MATERIAL AND METHODS HL-60 cells were treated with nicotinamide and divided into 0.1, 1, and 10 μmol/l groups. HL-60 cells without any administration were assigned as negative control (CT group). Glucolytic activity was evaluated by detecting lactic acid production, and glucose level was measured using glucose consumption assay. Apoptosis of HL-60 was examined using flow cytometry assay, when cells were cultured for 24 h. Expressions of sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator 1alpha (PGC-1alpha), and hypoxia-inducible factor-2alpha (HIF2alpha) were evaluated using a reverse transcription PCR assay and Western blotting assay, respectively. RESULTS Nicotinamide remarkably decreased lactic acid production and glucose levels in leukemia cells compared with that of the CT group (p<0.05). Nicotinamide significantly induced the apoptosis of HL-60 cells compared to that of the negative control group (p<0.05). Nicotinamide significantly inhibited the SIRT1/PGC-1alpha/HIF2alpha signaling pathway mRNAs compared to that of the CT group (p<0.05). Nicotinamide remarkably reduced mitochondrial regulatory factors SIRT1/PGC-1alpha expression compared to that in the CT group (p<0.05). Nicotinamide obviously downregulated HIF2alpha compared with that of the CT group (p<0.05). Moreover, all of the above nicotinamide-induced effects, including glycolytic activity, apoptosis, and expression of SIRT1/PGC-1alpha/HIF2alpha, were changed in a dose-dependent manner. CONCLUSIONS Nicotinamide can inhibit glycolysis of HL-60 cells by inhibiting the mitochondrial regulatory factor SIRT1/PGC-1alpha and suppressing transcription factor HIF2alpha.
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.