Xu, et al. aimed to investigate miRNA‑301a‑3p expression in Gastric Cancer progression and the molecular mechanisms that regulate NF‑κB signaling. Researchers found that miRNA‑301a‑3p expression was significantly higher in 30 cases of primary Gastric Cancer compared to matched normal tissues. High expression of miRNA‑301a‑3p in GC was associated with tumor invasion depth, lymph node metastasis, lymph node invasion, tumor metastasis, and a poorer prognosis.
NF-κB signaling promotes tumor cells to produce numerous tumorigenic factors, including the angiogenesis regulator, vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-2, MMP-9, the chemokines, interleukin (IL)-1, IL-8, tumor necrosis factor (TNF), IL-6 and monocyte chemoattractant protein-1 (MCP-1), and the anti-apoptotic factors, Bcl-xL and cellular inhibitor of apoptosis proteins (cIAPs), which are essential to tumor progression. Xu, et al. used HUABIO to show changes in the protein levels of NKRF, NF-κB, VEGF, MMP-2 and MMP-9 proteins after the GC cells were transfected with the miRNA-301a-3p inhibitor and mimic by western blot analysis.
These results demonstrated that the upregulation of miRNA-301a-3p contributed to tumor progression in Gastric Cancer by regulating NKRF expression, which led to the induction of NF-κB activation and tumor growth. Therefore, this NF-κB activation mechanism may be a target for therapeutic intervention in GC.
Antibodies Used:
EM1801-22 MMP-9 Monoclonal Antibody
M1310-2 GAPDH Monoclonal Antibody
Reference: