Silencing of nuclear factor kappa b 1 gene expression inhibits colony formation, cell migration and invasion via the downregulation of interleukin 1 beta and matrix metallopeptidase 9 in renal cell carcinoma.
Furthermore, we demonstrated that the higher bacterial invasion in human INT407 triggered higher levels of expression of major proinflammatory cytokines, such as IL- 1β and IL-6, and significant downregulation of IL-17A gene expression (P ≤ 0.05).
Cell migration and invasion abilities were determined using scratch-wound and Transwell invasion assays, respectively. mRNA and protein expression patterns of nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 (NLRP3), caspase-1 and IL-1β were detected using qRT-PCR, immunofluorescence and western blot.
The pro-tumorigenic roles of IL-1 were counteracted by its effects on myeloid cells, particularly neutrophils, where IL-1R1 ablation resulted in bacterial invasion into tumors, heightened inflammation and aggressive CRC progression.
Furthermore, increased NOD1 expression in the normal DSCs induced apoptosis and increased monocyte chemotactic protein-1 (MCP-1) and IL-1β (interleukin 1 beta) secretion but decreased their invasion capacity.
CTH promotes NF-κB nuclear translocation through H<sub>2</sub> S-mediated sulfhydration on cysteine-38 of the NF-κB p65 subunit, resulting in increased IL-1β expression and H<sub>2</sub> S-induced cell invasion.
Interleukin-1 (IL-1) and IL-12 cytokine family members cooperate at barrier tissues after microbial invasion, in human inflammatory diseases, and in antitumoral immunity.
Over-expression of PERP resulted in not only increasing SE adhesion and invasion but also triggering the production of IL-1β and IFN-α in SE infected dGCs, while knock-down PERP showed the opposite tendency (<i>P</i> < 0.01).
We show in a mouse model that maternally administrated IL-1 receptor antagonist (IRA; Kineret, or anakinra), following ZIKV exposure, can preserve placental function (by improving trophoblast invasion and placental vasculature), increase fetal viability, and reduce neurobehavioral deficits in the offspring.
Of note, IL-1β stimulation promoted cell migration and invasion mainly through COX-2 induction, but YAP inhibited this induction and thus cell migration and invasion.
Mesometrial tissues from seropositive dams were analyzed for expression of interleukin 1β, 6, and 10, TNF, TGF-β, follistatin-related protein 3, and inhibin beta A chain since these genes regulate extravillous trophoblast invasion.
Monolayer co-cultivation, agarose drop chemotaxis, and transwell assay were conducted to investigate the chemotaxis invasion and transendothelial migration ability of IL-1β-induced MSCs in response to CXCL9.
In cultures of primary FLS isolated from the AIA rats, Madec (10 and 30 μmol·L<sup>-1</sup>) was proven to considerably inhibit migration and invasion of FLS induced by interleukin 1β (IL-1β), but exhibiting no obvious effect on cell proliferation.
Stimulation with 10 <i>µ</i>g/ml PM2.5 increases the invasion ability of HeLa cells and promotes the expression of inflammatory cytokines IL-1 and IL-6.
IL-1 acts at different levels in tumor initiation and progression, including driving chronic non-resolving inflammation, tumor angiogenesis, activation of the IL-17 pathway, induction of myeloid-derived suppressor cells (MDSC) and macrophage recruitment, invasion and metastasis.
MiR-124a is of great significance for the onset of RA by inhibiting the proliferation and invasion of RASFs possibly through downregulating the expression of MMP3/13 and IL-1β.
We performed RNA sequencing of HuR-silenced microglia and found significant attenuation of lipopolysaccharide-induced IL-1β and TNF-α inflammatory pathways and other factors that promote microglial migration and invasion.