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ABSTRACT: The aim of this study was to investigate whether magnesium ascorbyl phosphate (MAP) and coenzyme Q10 (CoQ10) can protect keratinocytes against ultraviolet (UV)A irradiation by increasing the levels of glutathione (GSH). The cell survival fraction was 89.9% when the keratinocytes were irradiated with UVA at a dose of 4 J/cm2. The cell survival fractions were 48.4, 9.1 and 4.8%, at doses of 8, 16 and 32 J/cm2, respectively. MAP was added to the cells prior to UVA irradiation at a dose of 8 J/cm2 and then the cell viability was assayed. The cell survival fractions were 51.6, 55.5, 64.8 and 76.7%, when MAP was added at concentrations of 125, 250, 500 µM and 1 mM, respectively. The results showed that MAP is capable of protecting keratinocytes against UVA irradiation. The cell survival fractions were 77.2, 89.4 and 90.1%, when CoQ10 was added at concentrations of 2.5, 5 and 10 µM, respectively. The results revealed that CoQ10 is capable of protecting keratinocytes against UVA irradiation. At the same time, the levels of GSH within cells were detected. The level of GSH within cells was 0.3 mmol/g protein when the keratinocytes were irradiated with UVA at a dose of 8 J/cm2. We measured the levels of GSH within the cells after MAP or CoQ10 was added prior to UVA irradiation at a dose of 8 J/cm2. The levels of GSH within the cells were 0.344, 0.388, 0.456 and 0.5 mmol/g protein, when MAP was added at concentrations of 125, 250, 500 µM and 1 mM, respectively. The levels of GSH within the cells were 0.328, 0.35 and 0.394 mmol/g protein, when CoQ10 was added at concentrations of 2.5, 5 and 10 µM, respectively. These results imply that MAP and CoQ10 can protect the keratinocytes against UVA irradiation, possibly via increasing the levels of GSH.
Molecular Medicine Reports 05/2012; 6(2):375-8. · 0.42 Impact Factor
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ABSTRACT: To investigate how a complex network of CC chemokine ligands (CCLs) and their receptors influence the progression of tumor and metastasis.
In the present study, we used immunohistochemistry to examine the expression of CCL7, CCL8 and CCL21 in 194 gastric cancer samples and adjacent normal tissues. We analyzed their correlation with tumor metastasis, clinicopathologic parameters and clinical outcome.
We found that the higher expression of CCL7 and CCL21 in cancer tissues than in normal tissues was significantly correlated with advanced depth of wall invasion, lymph node metastasis and higher tumor node metastasis stage. Moreover, Kaplan-Meier survival analysis revealed that CCL7 and CCL21 overexpression in cancer tissues was correlated with poor prognosis.
These results suggest that overexpression of these two CC chemokine ligands is associated with tumor metastasis and serves as a prognostic factor in patients with gastric cancer.
World Journal of Gastroenterology 03/2012; 18(11):1249-56. · 2.47 Impact Factor
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ABSTRACT: Claudin-4 is a member of the claudin family, a large family of transmembrane proteins that are essential in the formation and maintenance of tight junctions. Matrix metal-loproteinase (MMP)-2 and -9 degrade type IV collagen of the extracellular matrix and basal membranes. Claudin-4 activates MMP-2, indicating that claudin-mediated increased cancer cell invasion may result from the activation of MMP proteins. In the present study, we used immunohistochemistry to examine the expression levels of claudin-4, MMP-2 and MMP-9 in 189 gastric cancer samples, and analyzed their correlation with tumor invasion, clinicopathologic parameters and clinical outcome. The relationship between claudin-4 expression and MMP-2 and -9 expression was also investigated. The expression of claudin-4 was found to be significantly higher in gastric cancer cases with advanced depth of wall invasion, lymph node metastasis, lymphatic invasion and higher TNM stage. Further analysis revealed claudin-4 expression to be significantly correlated with the expression of MMP-2 and -9. Kaplan-Meier survival analysis indicated that MMP-9 expression was correlated with poor prognosis. These results suggest that claudin-4 expression is associated with tumor invasion and with MMP-2 and -9 expression in gastric cancer. Additionally, MMP-9 expression was demonstrated to serve as a prognostic factor in patients with gastric cancer.
Experimental and therapeutic medicine 01/2010; 1(5):789-797.
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ABSTRACT: Matrix metalloproteinases (MMPs) MMP-2 and MMP-9 can degrade type IV collagen of extracellular matrix and basal membranes. Claudin-4 is a member of a large family of transmembrane proteins, claudins, essential in the formation and maintenance of tight junctions. Claudin-4 has been shown to activate MMP-2, indicating that claudin-mediated increased cancer cell invasion might be mediated through the activation of MMP proteins. To explore the roles of MMP-2, MMP-9 and claudin-4 in gastric cancer, we selected 88 cases and then analyzed the expression of these proteins using immunohistochemistry. We found that all of MMP-2, MMP-9 and claudin-4 expressions were significantly higher in intestinal-type than in diffuse-type gastric cancer. On further analysis, testing the relationship between MMP-2 and MMP-9 expression with claudin-4 expression, claudin-4 expression was significantly associated with MMP-9 expression, but not with MMP-2 expression. The results showed that MMP-2, MMP-9 and claudin-4 expression may be phenotypic features, distinguishing intestinal-type and diffuse-type gastric cancer. Possibly, claudin-4 played a role in determining MMP-9 activity which favored intestinal-type gastric cancer to distal metastasis.
Histology and histopathology 06/2008; 23(5):515-21. · 2.48 Impact Factor
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ABSTRACT: Our previous microarray analysis of gastric cancer found that claudin-4 was differentially expressed between intestinal-type gastric cancer (IGC) and diffuse-type gastric cancer (DGC). Claudin-4 is a member of a large family of transmembrane proteins, claudins, essential in the formation and maintenance of tight junctions. To explore the roles of claudin-4 in the two histologically distinct types of gastric cancer, we selected 45 IGC and 48 DGC cases and then analyzed the expression of the protein using immunohistochemistry. We found that the overexpression of claudin-4 was greater in IGC than in DGC. A trend was observed between the overexpression of claudin-4 and lymph node metastasis, however, this association was not statistically significant. The results showed that the expression of claudin-4 was lower in DGC. Possibly it played a role in determining the diffuse phenotype and loose cohesion of cells in DGC in a similar manner as E-cadherin.
Oncology Reports 11/2006; 16(4):729-34. · 1.84 Impact Factor
