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Vanadium Compounds as Pro-Inflammatory Agents: Effects on Cyclooxygenases.

Korbecki J, Baranowska-Bosiacka I, Gutowska I, Chlubek D - Int J Mol Sci (2015)

Bottom Line: We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling.We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2.For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Medical Chemistry, Pomeranian Medical University, Powstańców Wlkp. 72 Av., 70-111 Szczecin, Poland. jan.korbecki@onet.eu.

ABSTRACT
This paper discusses how the activity and expression of cyclooxygenases are influenced by vanadium compounds at anticancer concentrations and recorded in inorganic vanadium poisonings. We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling. We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2. For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

No MeSH data available.


Related in: MedlinePlus

The mechanism of the activation of mitogen-activated protein kinase (MAPK) cascades in the expression of COX-2 by vanadium compounds. Vanadium compounds are the inhibitors of PTPs which directly affect the activity of Src, as well as epidermal growth factor receptor (EGFR) and MAPK. The activation of Src results in the phosphorylation of tyrosine residues on PLCγ. This process causes the binding of PLCγ to phosphorylated EGFR or to another receptor. This is followed by the transmission of the signal to PKC and consequently the activation of MAPK cascades. Vanadium compounds can activate MAPK cascades also by EGFR, independently of PLCγ.
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ijms-16-12648-f003: The mechanism of the activation of mitogen-activated protein kinase (MAPK) cascades in the expression of COX-2 by vanadium compounds. Vanadium compounds are the inhibitors of PTPs which directly affect the activity of Src, as well as epidermal growth factor receptor (EGFR) and MAPK. The activation of Src results in the phosphorylation of tyrosine residues on PLCγ. This process causes the binding of PLCγ to phosphorylated EGFR or to another receptor. This is followed by the transmission of the signal to PKC and consequently the activation of MAPK cascades. Vanadium compounds can activate MAPK cascades also by EGFR, independently of PLCγ.

Mentions: Through the inhibition of PTP activity, vanadium compounds increase the overall phosphorylation on the EGFR tyrosine residues [47]. This causes the signal transduction to MAPK cascade (Figure 3). In human A431 squamous carcinoma cells the highest susceptibility to vanadate is shown by EGFR Tyr992, the phosphorylation of which results in the signal transmission by PLCγ-PKC to MAPK cascades [47]. Nevertheless, PLCγ-dependent pathway is not the only route of MAPK cascades activation. In addition, in the human airway, epithelial BEAS-2B cells vanadium compounds activate Ras, which results in the transmission of the signal to MAPK kinase cascades and NF-κB [70,71].


Vanadium Compounds as Pro-Inflammatory Agents: Effects on Cyclooxygenases.

Korbecki J, Baranowska-Bosiacka I, Gutowska I, Chlubek D - Int J Mol Sci (2015)

The mechanism of the activation of mitogen-activated protein kinase (MAPK) cascades in the expression of COX-2 by vanadium compounds. Vanadium compounds are the inhibitors of PTPs which directly affect the activity of Src, as well as epidermal growth factor receptor (EGFR) and MAPK. The activation of Src results in the phosphorylation of tyrosine residues on PLCγ. This process causes the binding of PLCγ to phosphorylated EGFR or to another receptor. This is followed by the transmission of the signal to PKC and consequently the activation of MAPK cascades. Vanadium compounds can activate MAPK cascades also by EGFR, independently of PLCγ.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4490466&req=5

ijms-16-12648-f003: The mechanism of the activation of mitogen-activated protein kinase (MAPK) cascades in the expression of COX-2 by vanadium compounds. Vanadium compounds are the inhibitors of PTPs which directly affect the activity of Src, as well as epidermal growth factor receptor (EGFR) and MAPK. The activation of Src results in the phosphorylation of tyrosine residues on PLCγ. This process causes the binding of PLCγ to phosphorylated EGFR or to another receptor. This is followed by the transmission of the signal to PKC and consequently the activation of MAPK cascades. Vanadium compounds can activate MAPK cascades also by EGFR, independently of PLCγ.
Mentions: Through the inhibition of PTP activity, vanadium compounds increase the overall phosphorylation on the EGFR tyrosine residues [47]. This causes the signal transduction to MAPK cascade (Figure 3). In human A431 squamous carcinoma cells the highest susceptibility to vanadate is shown by EGFR Tyr992, the phosphorylation of which results in the signal transmission by PLCγ-PKC to MAPK cascades [47]. Nevertheless, PLCγ-dependent pathway is not the only route of MAPK cascades activation. In addition, in the human airway, epithelial BEAS-2B cells vanadium compounds activate Ras, which results in the transmission of the signal to MAPK kinase cascades and NF-κB [70,71].

Bottom Line: We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling.We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2.For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Medical Chemistry, Pomeranian Medical University, Powstańców Wlkp. 72 Av., 70-111 Szczecin, Poland. jan.korbecki@onet.eu.

ABSTRACT
This paper discusses how the activity and expression of cyclooxygenases are influenced by vanadium compounds at anticancer concentrations and recorded in inorganic vanadium poisonings. We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling. We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2. For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

No MeSH data available.


Related in: MedlinePlus