Decavanadate Inhibits the Cell-Free Activation of Neutrophil NADPH Oxidase without Affecting Tyrosine Phosphorylation.

Okamura, Nobuyuki; Sakai, Tomoko; Nishimura, Yuko; Sakai, M.; Araki, Shiho; Yamaguchi, M.; Ishibashi, Shun

doi:10.1248/bpb.22.799

Cited by 2 publications

(2 citation statements)

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“…Several studies report that DV has a strong inhibitory effect on several enzymes, when compared to other oligomers: − inhibition of Ca 2+ ATPase, − Na,K-ATPase, muts ATPase, myosin ATPase, − acid phosphatase A, and other biological targets. − It has also been recently reported that DV can act as an insulin mimetic agent. , Aureliano et al have formulated the hypothesis that mytochondria might be a target for DV species . A complete review of biological activities of DV is given in a recent review of Aureliano et al…”

Section: Introductionmentioning

confidence: 99%

Electronic Properties of a Cytosine Decavanadate: Toward a Better Understanding of Chemical and Biological Properties of Decavanadates

Bošnjaković-Pavlović

Biré

Tomaz³

et al. 2009

Inorg. Chem.

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We have synthesized and crystallized a cytosine-decavanadate compound, Na(3) [V(10)O(28)] (C(4)N(3)OH(5))(3)(C(4)N(3)OH(6))(3).10H(2)O, and its crystal structure has been determined from a single-crystal X-ray diffraction. A high resolution X-ray diffraction experiment at 210 K (in P1 space group phase) was carried out. The data were refined using a pseudo-atom multipole model to get the electron density and the electrostatic properties of the decavanadate-cytosine complex. Static deformation density maps and Atoms in Molecules (AIM) topological analysis were used for this purpose. To get insight into the reactivity of the decavanadate anion, we have determined the atomic net charges and the molecular electrostatic potential. Special attention was paid to the hydrogen bonding occurring in the solid state between the decavanadate anion and its environment. The comparison of the experimental electronic characteristics of the decavanadate anions to those found in literature reveals that this anion is a rigid entity conserving its intrinsic properties. This is of particular importance for the future investigations of the biological activities of the decavanadate anion.

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Section: Introductionmentioning

confidence: 99%

Electronic Properties of a Cytosine Decavanadate: Toward a Better Understanding of Chemical and Biological Properties of Decavanadates

Bošnjaković-Pavlović

Biré

Tomaz³

et al. 2009

Inorg. Chem.

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“…Activation of NOX is coupled with stimulation of various cell membrane receptors as growth factors (14,15). Upon binding to growth factors, receptor tyrosine kinase (RTK) phosphorylates tyrosine residues in its intracellular domain, which then activates downstream signaling molecules such as PI3K/protein kinase B (Akt) and MAPKs.…”

Section: Introductionmentioning

confidence: 99%

Dual Inhibition of NOX2 and Receptor Tyrosine Kinase by BJ-1301 Enhances Anticancer Therapy Efficacy via Suppression of Autocrine-Stimulatory Factors in Lung Cancer

Gautam

Regmi

et al. 2017

Molecular Cancer Therapeutics

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NADPH oxidase-derived reactive oxygen species (ROS) potentiate receptor tyrosine kinase (RTK) signaling, resulting in enhanced angiogenesis and tumor growth. In this study, we report that BJ-1301, a hybrid of pyridinol and alpha-tocopherol, exerts anticancer effects by dual inhibition of NADPH oxidase and RTK activities in endothelial and lung cancer cells. BJ-1301 suppresses ROS production by blocking translocation of NADPH oxidase cytosolic subunits to the cell membrane, thereby inhibiting activation. The potency of RTK inhibition by BJ-1301 was lower than that of sunitinib (a multi-RTK inhibitor), but the inhibition of downstream signaling pathways (e.g., ROS generation) and subsequent biological changes (e.g., NOX2 induction) by BJ-1301 was superior. Consistently, BJ-1301 inhibited cisplatin-resistant lung cancer cell proliferation more than sunitinib did. In xenograft chick or mouse tumor models, BJ-1301 inhibited lung tumor growth, to an extent greater than that of sunitinib or cisplatin. Treatments with BJ-1301 induced regression of tumor growth, potentially due to downregulation of autocrine-stimulatory ligands for RTKs, such as TGFα and stem cell factor, in tumor tissues. Taken together, the current study demonstrates that BJ-1301 is a promising anticancer drug for the treatment of lung cancer. .

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Decavanadate Inhibits the Cell-Free Activation of Neutrophil NADPH Oxidase without Affecting Tyrosine Phosphorylation.

Cited by 2 publications

References 1 publication

Electronic Properties of a Cytosine Decavanadate: Toward a Better Understanding of Chemical and Biological Properties of Decavanadates

Electronic Properties of a Cytosine Decavanadate: Toward a Better Understanding of Chemical and Biological Properties of Decavanadates

Dual Inhibition of NOX2 and Receptor Tyrosine Kinase by BJ-1301 Enhances Anticancer Therapy Efficacy via Suppression of Autocrine-Stimulatory Factors in Lung Cancer

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