Growth suppression and cell death by pyridoxal is dependent on p53 in the human breast cancer cell line MCF-7

Vitamin B 6 compound, pyridoxine (PN), has shown antitumor action. Our previous experiments showed that PN induces expression of insulin-like growth factor binding protein-3 to arrest proliferation and induce cell death. This induction is inhibited by the p53-specific inhibitor pifithrin-α. Here, we...

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Veröffentlicht in:Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2015, Vol.79 (1), p.124-129
Hauptverfasser: Minamino, Masaki, Oka, Tatsuzo, Kanouchi, Hiroaki
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Sprache:eng
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Zusammenfassung:Vitamin B 6 compound, pyridoxine (PN), has shown antitumor action. Our previous experiments showed that PN induces expression of insulin-like growth factor binding protein-3 to arrest proliferation and induce cell death. This induction is inhibited by the p53-specific inhibitor pifithrin-α. Here, we report that another B 6 compound, pyridoxal (PL), strongly inhibited MCF-7 cell growth compared to PN. PL induced the G 0 /G 1 arrest and the accumulation of subG1 population. Although p53 mRNA was not changed by PL, 0.5 mM PL increased the protein level in MCF-7 cells. The cell growth suppression by 0.5 mM PL did not occur when p53 expression was knocked down using siRNA. Together, these data suggest that PL accumulate p53 and PL-induced cell growth suppression is dependent on p53 in MCF-7 breast cancer cells. Effect of PL on proliferation and viability under the p53 knockdown condition. PL significantly decreased cell growth and cell viability. These decreasing were reduced in p53 knockdown condition
ISSN:0916-8451
1347-6947
DOI:10.1080/09168451.2014.952618