Comparisons of uptake and cell surface binding among pyridoxal, pyridoxine, and pyridoxamine in RAW264.7 cells

Kanouchi, Hiroaki; Shibuya, Mayumi; Tsukamoto, Shuntaro; Fujimura, Yoshinori; Tachibana, Hirofumi; Yamada, Koji; Oka, Tatsuzo

doi:10.1016/j.nut.2009.08.005

Cited by 10 publications

(9 citation statements)

References 19 publications

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“…We recently found that PL remarkably increases IGFBP1 mRNA whereas no other B 6 -vitamers have a similar effect (11). PL can freely pass through the cell membrane, and only PL is reported to interact with the cell surface of RAW264.7 cells cultured in culture medium treated with B 6 -vitamers (i.e., PL, PM, PN and PLP) (17,18). Therefore, the stimulation of p21 mRNA expression might be related to the cell surface interaction and penetration of PL.…”

Section: Discussionmentioning

confidence: 99%

Vitamin B6 activates p53 and elevates p21 gene expression in cancer cells and the mouse colon

et al. 2014

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Abstract. Increasing evidence indicates vitamin B 6 acts as a protective factor against colon cancer. However, the mechanisms of the effect of vitamin B 6 are poorly understood. The present preliminary study using DNA microarray and realtime PCR indicates p21 mRNA is upregulated in human colon carcinoma (HT29) cells exposed to pyridoxal (PL, 500 µM). A similar effect was observed in human epithelial colorectal adenocarcinoma (Caco2) cells, human colon adenocarcinoma (LoVo) cells, human embryonic kidney (HEK293T) cells, and human hepatoma (HepG2) cells. Adding other B 6 -vitamers such as pyridoxal 5'-phosphate (PLP), pyridoxine (PN), and pyridoxamine (PM) caused no such effect. In order to understand the mechanism of higher mRNA expression of p21 by PL, effect of PL on the p53 activation was examined (the upstream factor for p21 mRNA transcription) in HT29 cells, LoVo cells, and HepG2 cells. PL increased the phosphorylated p53 protein levels (active form) in whole-cell lysates and the nuclei of the cells. Noteworthy, the consumption of a vitamin B 6 -deficient diet for 5 weeks significantly reduced p21 mRNA levels and tended to reduce phosphorylated p53 protein levels (P=0.053) in the colons of mice compared to a diet with adequate vitamin B 6 . Thus, these results suggest vitamin B 6 plays a role in increasing p21 gene expression via p53 activation in several cancer cells and the mouse colon.

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Section: Discussionmentioning

confidence: 99%

Vitamin B6 activates p53 and elevates p21 gene expression in cancer cells and the mouse colon

et al. 2014

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“…Our previous study showed that the inhibitory effect of PL on the LPS-induced expression of iNOS and COX-2 in RAW264.7 cells was stronger compared with PLP (9). Kanouchi et al (30) showed that when RAW264.7 cells were cultured in a culture medium treated with the B6 vitamers PL, PM, PN or PLP, only PL interacted with the cell surface. PL is known as a primary form of transport in blood and is capable of freely passing through the cell membrane, while PLP cannot easily cross the cell membrane and must be hydrolyzed by alkaline phosphatase into PL (31)(32)(33).…”

Section: Discussionmentioning

confidence: 99%

High concentrations of pyridoxal stimulate the expression of IGFBP1 in HepG2 cells through upregulation of the ERK/c-Jun pathway

Zhang

Suidasari

Hasegawa

et al. 2013

Molecular Medicine Reports

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Abstract. Increasing evidence suggests that dietary vitamin B6 is linked to the prevention of cancer and cardiovascular disease. However, the molecular mechanisms involved in this process are not yet understood. Preliminary results in the current study indicated, following DNA microarray analysis and quantitative PCR, that insulin-like growth factor-binding protein 1 (IGFBP1) mRNA is upregulated in HT29 colon carcinoma cells exposed to pyridoxal (PL, 500 µM). IGFBP1 is secreted from the liver and is hypothesized to exert a protective role in the development of cancer and cardiovascular disease. Thus, further experiments were performed to investigate the effect of PL on the expression of IGFBP1 in HepG2 hepatocellular carcinoma cells. The addition of PL (500 µM) markedly increased the expression of IGFBP1 mRNA in HepG2 cells at 6, 12 and 24 h (P<0.01), whereas other vitamers (500 µM), including pyridoxal 5'-phosphate (PLP), pyridoxine (PN) and pyridoxamine (PM), caused no such effect. The expression of the IGFBP1 protein in the cell lysate and culture medium was elevated in the presence of PL. PL elevated expression of the active form of ERK1 protein, p-ERK1, and the p-c-Jun protein, a downstream factor of ERK. Furthermore, IGFBP1 expression, elevated by PL, was suppressed by PD98059, an ERK inhibitor. Higher expression of IGFBP1 protein by PL was suppressed by cycloheximide. These results suggest that PL may induce the expression of IGFBP1 in hepatoma cells via a mechanism involving the ERK/c-Jun pathway.

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“…Therefore, the antitumor effect of PL appears to be strong. However, in RAW264.7 cells, the addition of PL could not increase intracellular PLP concentration (12). The cell inhibitory effect of PL might not be dependent on PLP.…”

Section: Discussionmentioning

confidence: 80%

“…PN did not suppress the melanogenesis compared with vitamin B 6 free condition. A previous study showed that PL suppressed lipopolysaccharide-stimulating COX-2 expression more strongly than PN in RAW264.7 murine macrophage cells (12). PL might inhibit IBMX-stimulating tyrosinase expression compared with PN.…”

Section: Discussionmentioning

confidence: 88%

The effects of vitamin B6 compounds on cell proliferation and melanogenesis in B16F10 melanoma cells

et al. 2018

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Abstract. B16F10 murine melanoma cells are frequently used for the study of cancer and melanogenesis. The cells are usually cultured in Dulbecco's Modified Eagle Medium, with the addition of 20 µM pyridoxal (PL) or pyridoxine (PN) for vitamin B 6 . The difference between these vitamin B 6 compounds is thought not to affect cell proliferation, whereas their influence on other physiological effects is poorly understood. In the present study, the effects of PL and PN on cell proliferation and melanogenesis in B16F10 cells were compared. At 500 µM PL significantly suppressed cell growth but the growth inhibitory effect of PN was weak. Although neither of the vitamin B 6 compounds affected cell growth at 20 µM, melanogenesis was suppressed by 20 µM PL compared with the effect of PN. In addition, the expression levels of tyrosinase, which is the rate-limiting enzyme, correlated with the melanin content. The results of the present study indicate that PL may be more useful for melanoma therapy and suppression of skin pigmentation than PN. The results also signify the importance of medium selection for cell culture.

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Comparisons of uptake and cell surface binding among pyridoxal, pyridoxine, and pyridoxamine in RAW264.7 cells

Cited by 10 publications

References 19 publications

Vitamin B6 activates p53 and elevates p21 gene expression in cancer cells and the mouse colon

Vitamin B6 activates p53 and elevates p21 gene expression in cancer cells and the mouse colon

High concentrations of pyridoxal stimulate the expression of IGFBP1 in HepG2 cells through upregulation of the ERK/c-Jun pathway

The effects of vitamin B6 compounds on cell proliferation and melanogenesis in B16F10 melanoma cells

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