Although the major observations were mediated by Ch/γ-PGA NPs, the incorporation of IFN-γ into NPs potentiated the expression of CD40 and CD86, and the impairment of colorectal cancer cell invasion.
Collectively, our results demonstrate that IFNγ inhibits fibroblast-leading tumor cell invasion by inhibiting the motility of fibroblasts and their adhesion with tumor cells.
In this study, we found a vital role of IFN-γ in enhancing proliferation, inhibiting apoptosis, and promoting cell migration and invasion in gastric cancer cells SGC-7901 and MGC-803.
Syndecan-binding protein (SDCBP), which is induced by tumor necrosis factor-α and interferon-γ, controls the proliferation and invasion of several different types of cancer cells.
This study addressed the hypothesis that previous establishment of regional EAE would determine subsequent tissue localization of new T-cell invasion and associated symptoms regardless of the presence or absence of IFN-γ production.
In conclusion, our study demonstrated that knockdown of hTERT and concurrent treatment with IFN-gamma effectively inhibited cell proliferation, migration, and invasion in glioblastoma cells through downregulation of the molecules involved in these processes and cell cycle inhibition.
This correlation suggests that IFN-gamma-mediated cell activation is a genetically controlled quantitative trait and that it determines the outcome of mycobacterial invasion in man.