All the above results demonstrated that p54nrb slightly inhibited THP1 cell proliferation, but significantly promoted migration, invasion and release of TNF-α induced by LPS in THP1 cells.
GC patients who have both IL-1β-31 CC and IL-1β-511 TT genotypes and have at least one of protective genotypes (IL-1β-31 CC, IL-1β-511 TT, TNF-α-857 T carrier) were also associated with better prognostic factors, such as lymphatic and venous invasion better survival.
PTEN knockdown increased the invasion and migration of CRC cells and the addition of medium containing tumor necrosis factor-alpha (TNF-alpha) further enhanced the migration and invasion.
We conclude the milieu cytokine, TNF-alpha, has the capacity to provide stimulation of events related to early invasion of oral cavity cancer, as judged by its ability to stimulate MMP-9.
In our study, we found that apomorphine (APO), one of the most commonly prescribed DR agonists, inhibited TNF-α-induced matrix metalloprotease-9 (MMP-9) expression and cell invasion in MCF-7 human breast carcinoma cells through DR-independent pathways.
In conclusion, our findings show that M2-medium enriched in TNFα and LTD<sub>4</sub> promote colon cancer cell invasion via MMP-9 expression and activation and the induction of EMT.
In addition, small interfering RNA against FAK drastically suppressed the TNF-alpha-dependent production of MMP-9 and inhibited the TNF-alpha-dependent invasion of CCKS1.
We found that Zyflamend inhibited receptor activator of NF-kappa B ligand-induced osteoclastogenesis, suppressed tumor necrosis factor (TNF)-induced invasion, and potentiated the cytotoxicity induced by TNF and chemotherapeutic agents, all of which are known to require NF-kappa B activation.
Taken together, mammary tumor cell invasiveness was stimulated by TNF-α induced activation of Hh signaling; these effects were abrogated by daidzein, which suppressed Gli1 activation, thereby inhibiting migration and invasion.
In the present study, we demonstrate that NF-kappaB, whether activated by recombinant human tumor necrosis factor (TNF)-alpha or by ectopic expression of the p65 subunit, is involved in extracellular matrix adhesion and invasion of osteotropic PC-3 and C4-2B, but not LNCaP, cells.
Recent evidence suggests that inflammation-related cytokine tumor necrosis factor-alpha (TNF-α) is implicated in tumor invasion and metastasis, but the mechanism of its involvement remains elusive.
In the invasive MDA-MB-231 cells, Rac3 inhibition caused a marked reduction of both invasion (40%) and cell adhesion to collagen (84%), accompanied by an increase in TNF-induced apoptosis (72%).
In the present study, we aimed to investigate the function of SETD7 in regulating ASM cell proliferation and invasion induced by tumor necrosis factor (TNF)-α in vitro.
β4GalT1 promoted cell invasion, MMP-3 production, and the secretion of TNF-α, IL-1β, and IL-6. si-TNF-α attenuated the β4GalT1-enhanced cell invasion and inflammatory factor secretion in OA-FLS.
Exploration on the potential mechanism underlying meningoencephalitis demonstrated that CEC-GZL17 infection significantly increases TNF-α expression and inhibits ZO-1 and occludin expressions in brain tissue, indicating that the E coli likely use the mechanism to penetrate the blood-brain barrier via disrupting tight junction architecture, thus leading to the invasion to brain tissue.
IFN-gamma abolished the enhancement of MMP-13 and MMP-1 expression by transforming growth factor-beta (TGF-beta) and tumor necrosis factor-alpha (TNF-alpha), and inhibited invasion of A-5 cells through type I collagen.
These effects correlated with enhancement of apoptosis induced by TNF and suppression of TNF-induced invasion and receptor activator of NF-kappaB ligand-induced osteoclastogenesis.
Silencing and overexpression experiments indicated that TLR2 promotes ICC migration and invasion, induces the expression of epithelial-to-mesenchymal transition (EMT) markers, and upregulates the proinflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β concomitant with the activation of NF-κB signaling.
Western blotting, immunofluorescence, qRT-PCR, wound healing scratch and invasion assay, and chromatin immunoprecipitation assays were used to study the combined roles of EGF and TNFα in the motility of HCC cells in vitro.
The Th1-cytokines produced by T cells, such as INF-γ, IL-2, and TNF-α, not only limit the invasion of <i>M. tuberculosis</i> but also eliminate the pathogen at the site of infection.