A panel of GC cell lines showed reduced proliferation, invasion, and migration capacities after RNA-mediated knockdown of EphA8, concomitant with downregulation of the proliferation-related proteins (cyclin A, cyclin D1, and cyclin-dependent kinase 4) and the metastasis-related (matrix metalloproteinases MMP2, and MMP9).
Moreover, H19 depletion increased AMPK activation and decreased MMP9 expression, and metformin could not further activate AMPK or decrease MMP9 in H19 knocked-down gastric cancer cells.
Subsequently, MMP9, a key molecule in gastric cancer, was explored as one of target genes that were transcribed by VGLL1-TEAD4 complex, a component of the transcription factor.
Combined detection of negative marker PGC and positive markers MG7-Ag and MMP9 could be used as a potential follow-up panel for monitoring dynamical progression of AG and improving the detection efficiency of high-risk individuals of gastric cancer, and then taking necessary interventions on the target population.
These results suggest that TNF-α-induced MMP-9 secretion from mesothelial cells plays an important role in the metastatic dissemination of gastric cancer.
Positive expression of matrix metalloproteinase-9 and vascular endothelial growth factor and negative expression of E-cadherin were malignant markers for gastric cancer.
Additionally, PTEN knockdown promoted the migration and invasion of cells and caused an obvious increase in p-AKT, p-GSK-3β, β-catenin, E-cadherin, MMP-7, MMP-2, and MMP-9 in gastric cancer cells.
A variety of studies have observed that the single nucleotide polymorphisms (SNPs) matrix metalloproteinase-9 (MMP-9) gene may be associated with the risk of gastric cancer(GC), and a cytosine (C) to thymine (T) mutation at the -1562 site of the MMP-9 gene promoter is reported to be closely related to the susceptibility.
GS-5745, a potent, highly selective humanized monoclonal antibody inhibitor of MMP9, has shown promise in treating ulcerative colitis and gastric cancer.
Chi‑square tests suggested that STIM1 expression in GC tissues was significantly associated with E‑cadherin (P<0.001) and β‑catenin (P<0.001), whereas no association was observed between STIM1 and MMP‑9 expression (P>0.05).
The haplotype MMP9-1562C/279Q/668Q was more frequently observed in individuals whose both parents had a history of GC and in individuals for whom one parent and their sibling(s) had a history of GC compared with those with no family history (OR 3.35, 95 % CI 0.75-14.96 and OR 3.51, 95 % CI 1.35-9.15 respectively).
101 cases of gastric cancer specimens were utilized to identify the protein expression of NDRG1 and MMP-9 by immunohistochemistry, their clinical significance was also analyzed.
First, we sought to investigate under a case-control design the association between the functional -1562C/T polymorphism in the promoter region of MMP-9 and gastric cancer (GC) in a Turkish sample.
A dose-dependent elevation of MMP-9 activity was observed by NT treatment in gastric cancer cells (MKN-1 and MKN-45) compared to untreated gastric cancer and normal epithelial cell (HFE-145).
Several genetic polymorphisms have been identified that show allele specific effects on MMP9 regulation and are associated with gastric cancer, the fourth most common malignancy in the world.
Fz2 shRNA suppressed cell proliferation and motility of MKN45 and MKN74 cells, and downregulated cyclin D1 and MMP-9 expression in these GC cell lines.