Expression of Matrix Metalloproteinase-9 in Gastric Cancer.

Background Matrix-metalloproteinase-9 (MMP-9) is expressed by a wide range of cells and plays a significant role in the regulation of the tumor microenvironment of various cancers including gastric cancer. This study aims at the correlation of MMP-9 expression in gastric cancer with existing prognostic factors. Methods The MMP-9 expression in gastric cancer was identified by immunohistochemistry using a monoclonal antibody in paraffin-embedded sections, correlated with various clinicopathological parameters, and statistically analyzed. Results MMP-9 expression in gastric cancer was significantly correlated with the grade, depth of invasion, and TNM stage (p-value = 0.003, 0.019, and 0.025, respectively). A significant difference in expression between tumor tissue and adjacent gastric mucosa (p-value = 0.000) was also observed. 100% negative expression was found in well-differentiated tumors and early gastric carcinoma (T1). Conclusion The study results suggest that MMP-9 expression could be a potential biomarker of aggressive gastric cancer and candidates for the possible diagnostic and prognostic tool.

EGCG mediated downregulation of NF-AT and macrophage infiltration in experimental hepatic steatosis.

SCOPE: Increased fat consumption in industrialized countries has resulted in hepatic steatosis that upregulates atherogenic aspirant genes, leading to atherosclerosis and mortality. Although extensive studies have been carried out to elucidate the atheroprotective efficacy of epigallocatechin-3-gallate (EGCG), the effect of EGCG on hepatic steatosis has not been studied comprehensively. Hence, the current study was designed to find out the effect of EGCG on hepatic events that prelude atherosclerosis with special reference to macrophage infiltration. METHODS AND RESULTS: Male albino rats of Wistar strain were used in this study. Basic biochemical assays along with the protein expression of CAMs, NF-κB, TNF-α and NF-AT were assayed in the current study. EGCG supplementation significantly reverted the alterations in both biochemical and histological parameters and is shown to reduce the TNF-α mediated NF-AT expression and thereby its downstream targets like ICAM-1 and E-selectin expression to a greater extent than NF-κB mediated downstream targets like VCAM-1 and P-selectin in hypercholesterolemic rat liver. CONCLUSION: Our results suggest that EGCG influences the early events of atherosclerosis that occur; thereby modulating the NF-AT pathway and thereby mitigating the hypercholesterolemic stress.