Rare sugar d-allose strongly induces thioredoxin-interacting protein and inhibits osteoclast differentiation in Raw264 cells

Yamada, Kana; Noguchi, Chisato; Kamitori, Kazuyo; Dong, Yan; Hirata, Yuko; Hossain, Mohammad Akram; Tsukamoto, Ikuko; Tokuda, Masaaki; Yamaguchi, Fuminori

doi:10.1016/j.nutres.2011.12.010

Cited by 29 publications

(17 citation statements)

References 26 publications

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“…Previous studies have shown that MIF can interact with TXNIP to mitigate the inhibitory effect of TXNIP on NF-kB activity (30)(31)(32). TXNIP has also been shown to be expressed in osteoclasts and regulate RANKL-induced osteoclast formation (33,34). Using immunoprecipitation assays, we found that MIF is associated with the TXNIP-p65 complex upon RANKL stimulation, and this interaction was inhibited following treatment with 4-IPP ( Fig.…”

Section: -Ipp Inhibits Osteoclastogenesis Through Inhibition Of Nf-kmentioning

confidence: 60%

Macrophage migration inhibitory factor (MIF) inhibitor 4‐IPP suppresses osteoclast formation and promotes osteoblast differentiation through the inhibition of the NF‐κB signaling pathway

Zheng¹,

Gao²,

Jin³

et al. 2019

FASEB j.

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Current pharmacological intervention for the treatment of osteolytic bone diseases such as osteoporosis focuses on the prevention of excessive osteoclastic bone resorption but does not enhance osteoblast‐mediated bone formation. In our study, we have shown that 4‐iodo‐6‐phenylpyrimidine (4‐IPP), an irreversible inhibitor of macrophage migration inhibitory factor (MIF), can inhibit receptor activator of NF‐κB ligand (RANKL)‐induced osteoclastogenesis and potentiate osteoblast‐mediated mineralization and bone nodule formation in vitro. Mechanistically, 4‐IPP inhibited RANKL‐induced p65 phosphorylation and nuclear translocation by preventing the interaction of MIF with thioredoxin‐interacting protein—p65 complexes. This led to the suppression of late osteoclast marker genes such as nuclear factor of activated T cells cytoplasmic 1, resulting in impaired osteoclast formation. In contrast, 4‐IPP potentiated osteoblast differentiation and mineralization also through the inhibition of the p65/NF‐κB signaling cascade. In the murine model of pathologic osteolysis induced by titanium particles, 4‐IPP protected against calvarial bone destruction. Similarly, in the murine model of ovariectomy‐induced osteoporosis, 4‐IPP treatment ameliorated the bone loss associated with estrogen deficiency by reducing osteoclastic activities and enhancing osteoblastic bone formation. Collectively, these findings provide evidence for the pharmacological targeting of MIF for the treatment of osteolytic bone disorders.—Zheng, L., Gao, J., Jin, K., Chen, Z., Yu, W., Zhu, K., Huang, W., Liu, F., Mei, L., Lou, C., He, D. Macrophage migration inhibitory factor (MIF) inhibitor 4‐IPP suppresses osteoclast formation and promotes osteoblast differentiation through the inhibition of the NF‐κB signaling pathway. FASEB J. 33, 7667–7683 (2019). http://www.fasebj.org

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Section: -Ipp Inhibits Osteoclastogenesis Through Inhibition Of Nf-kmentioning

confidence: 60%

Macrophage migration inhibitory factor (MIF) inhibitor 4‐IPP suppresses osteoclast formation and promotes osteoblast differentiation through the inhibition of the NF‐κB signaling pathway

Zheng¹,

Gao²,

Jin³

et al. 2019

FASEB j.

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“…Both d-allose and d-glucose are monosaccharides, and d-allose is a C-3 epimer of d-glucose with 80% of the sweetness of sucrose. d-allose is one of many rare sugars that exist in very small quantities in nature (Izumori 2002), and our group has reported its unique properties such as anti-inflammatory (Gao et al 2013), anti-oxidative (Ishihara et al 2011), and inhibitory effects on osteoclast differentiation (Yamada et al 2012). d-allose inhibits the growth of many types of cancer cells, such as human hepatocellular carcinoma (HuH-7), HepG2, human gastric cancer (OVCAR3), and HeLa cells (Sui et al 2005a, b) and reduces the tumor volume in in vivo experiments (Hoshikawa et al 2010).…”

Section: Introductionmentioning

confidence: 99%

D-Allose Inhibits Cancer Cell Growth by Reducing GLUT1 Expression

Noguchi

Kamitori

Hossain

et al. 2016

Tohoku J. Exp. Med.

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Glucose is a major energy source for mammalian cells and is transported into cells via cell-specific expression of various glucose transporters (GLUTs). Especially, cancer cells require massive amounts of glucose as an energy source for their dysregulated growth and thus over-express GLUTs. d-allose, a C-3 epimer of d-glucose, is one of rare sugars that exist in small quantities in nature. We have shown that d-allose induces the tumor suppressor gene coding for thioredoxin interacting protein (TXNIP) and inhibits cancer cell growth by G1 cell cycle arrest. It has also been reported that GLUTs including GLUT1 are overexpressed in many cancer cell lines, which may contribute to larger glucose utilization. Since d-allose suppresses the growth of cancer cells through the upregulation of TXNIP expression, our present study focused on whether d-allose down-regulates GLUT1 expression via TXNIP expression and thus suppresses cancer cell growth. Western blot and real-time PCR analyses revealed that d-allose significantly induced TXNIP expression and inhibited GLUT1 expression in a dose-dependent manner in three human cancer cell lines: hepatocellular carcinoma (HuH-7), Caucasian breast adenocarcinoma (MDA-MB-231), and neuroblastoma (SH-SY5Y). In these cell lines, d-allose treatment inhibited cell growth. Importantly, d-allose treatment decreased glucose uptake, as measured by the uptake of 2-deoxy d-glucose. Moreover, the reporter assays showed that d-allose decreased the expression of luciferase through the hypoxia response element present in the tested promoter region. These results suggest that d-allose may cause the inhibition of cancer growth by reducing both GLUT1 expression and glucose uptake.

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“…Analysis of the function of D-psicose; Hossain et al, 2011 Analysis of the function of D-allose; Yamada et al, 2012, Kajikawa et al, 2010, Hirata et al, 2009 On the other hand, these are few papers analyzed by the viewpoint from consumers. The Rare Sugars are good for the health and are sold in the market as a sweetening, seasoning or functional ingredient for food.…”

Section: Introductionmentioning

confidence: 99%

Multivariate Analysis by Using Quantification Method Ⅱ on a Questionnaire Investigation for Rare Sugars

Ishii¹,

Takeyasu²,

Takeyasu³

et al. 2017

IBR

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The Rare Sugars exist naturally and have many kinds (more than 50). They have good effect for health such as prevention of increasing the blood-sugar level after eating, suppression of fat accumulation, suppression of increasing the blood pressure, and anti-oxidative effect etc. It is in the spotlight for many people especially for those who are in the metabolic syndrome. There are few related papers concerning the marketing research and its utilization of this matter. In this paper, a questionnaire investigation is executed in order to clarify consumers' current condition and their consciousness, and to seek the possibility of utilizing the Rare Sugars. Fundamental statistical analysis, Multivariate Analysis by Using Quantification Method Ⅱ are conducted based on that. Some interesting and instructive results were obtained.

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Rare sugar d-allose strongly induces thioredoxin-interacting protein and inhibits osteoclast differentiation in Raw264 cells

Cited by 29 publications

References 26 publications

Macrophage migration inhibitory factor (MIF) inhibitor 4‐IPP suppresses osteoclast formation and promotes osteoblast differentiation through the inhibition of the NF‐κB signaling pathway

Macrophage migration inhibitory factor (MIF) inhibitor 4‐IPP suppresses osteoclast formation and promotes osteoblast differentiation through the inhibition of the NF‐κB signaling pathway

D-Allose Inhibits Cancer Cell Growth by Reducing GLUT1 Expression

Multivariate Analysis by Using Quantification Method Ⅱ on a Questionnaire Investigation for Rare Sugars

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