Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is an attractive anticancer agent which can induce apoptosis in tumor cells without causing cytotoxicity to normal cellsHowever, resistance to TRAIL is often observed in some tumor cells, including nonsmall cell lung cancers, which may limit its cytotoxic efficacy in cancer treatmentThe combination treatment of TRAIL and herbal medicines, particularly <i>Coptidis Rhizoma</i> (CR) and <i>Curcumae longae Rhizoma</i> (CLR), can induce the synergistic cytotoxic effects against TRAIL-resistant A549 cells, indicating that TRAIL resistance was reduced by combination therapy.
In both melanoma and lung cancer cells, MEKi increased cell-surface expression of TNFα receptor 1 (TNFR1), which enhanced NF-κB activation and augmented expression of genes regulated by TNFα and IFNγ.
To evaluate for synergy between ART and the SMAC mimetic Debio 1143 and the dependence upon CD8<sup>+</sup> T cells and TNFα, we used LLC-OVA syngeneic mouse model of lung cancer and treated them with Debio 1143 and/or ART (30 Gy) with or without anti-CD8, anti-TNFα, or anti-IFNγ antibodies.
The purpose of this study was to investigate whether BrMC inhibits lung cancer stemness of H460 cells induced by inflammatory factors (TGF-β combined with TNF-α) and its potential mechanism.
We examined the association between three inflammatory markers (Interleukin (IL)-6, C-reactive protein (CRP), tumor necrosis factor (TNF)-α) and incident lung cancer using baseline, updated, and averaged inflammatory measures in older adults.
Statistically significant differences were identified between the two groups in transferrin and TNFα levels, as well as in TIBC; all three parameters were lower in the group consisting of COPD patients diagnosed with lung cancer (P<0.01).
TNF-α receptor-associated factor (TRAF)-interacting protein with a forkhead-associated (FHA) domain (TIFA) may mediate the impact of TRAF on the development of lung cancer.
We suggest concomitant EGFR and TNF inhibition as a potentially new treatment approach that could be beneficial for a majority of lung cancer patients.
The results from the present study revealed that the expression of IFN-γ, interleukin (IL)-2, tumor necrosis factor-α and IL-12 of PBMCs from patients with LC and healthy donors were significantly increased following treatment with rMBP-NAP (P<0.05).
We and others have previously identified a novel susceptibility gene <i>TNFRSF19</i>, which encodes an orphan member of the TNF receptor superfamily known to be associated with nasopharyngeal carcinoma (NPC) and lung cancer risk.
Bio informatics analysis of 982 lung cancer patients revealed that higher expression of TNF- α was associated with low risk of cancer progression while overexpression of IGF-1 was correlated with high risk.
Here, we report that Gd@C<sub>82</sub>(OH)<sub>22</sub> promote the binding activity of tumor necrosis factor (TNFα) to tumor necrosis factor receptors 2 (TNFR2), activate TNFR2/p38 MAPK signaling pathway to increase cellular collagen expression in fibrosarcoma cells and human primary lung cancer associated fibroblasts isolated from patients.
SASP components tumor necrosis factor-α and intercellular adhesion molecule-1 are required for NK cell surveillance of drug-treated tumor cells, which contributes to tumor regressions and prolonged survival in a KRAS-mutant lung cancer mouse model.
Tumor necrosis factor superfamily 15 promotes lymphatic metastasis via upregulation of vascular endothelial growth factor-C in a mouse model of lung cancer.
CD44 silencing decreases the expression of stem cell-related factors induced by transforming growth factor β1 and tumor necrosis factor α in lung cancer: Preliminary findings.
MSCs significantly augmented lung cancer metastasis, attenuate concentrations of proinflammatory cytokines (TNF-<i>α</i>, IL-17), and increase levels of immunosuppressive IL-10, nitric oxide, and kynurenine in sera of LLC1-treated mice.
Conditional logistic regression models adjusting for serum cotinine concentrations were used to estimate odds ratios for lung cancer risk associated with concentrations of interleukin (IL)-1β, IL-2, IL-6, IL-8, IL-10, IL-12, interferon γ, tumor necrosis factor α, and granulocyte-macrophage colony-stimulating factor.
Especially, SAHA increased the expression level of TNF-α receptor 1 (TNFR1), especially acetylation of the region of TNFR1 promoter -223/-29 in lung cancer cells.
Astragalin-induced cell death is caspase-dependent and enhances the susceptibility of lung cancer cells to tumor necrosis factor by inhibiting the NF-кB pathway.