Drug resistance in cells is a major impedance to successful treatment of lung cancer.Taxus chinensis var. inhibits the growth of tumor cells and promotes the synthesis of interleukins 1 and 2 and tumor necrosis factor, enhancing immune function.
Moreover, CYLD-overexpressed lung cancer cells were treated with 10 <i>μ</i>M of z-VAD-fmk for 12 hours and the result revealed that TNF-<i>α</i>-induced cell necrosis was significantly enhanced.
In conclusion, our findings demonstrate that ATM, which could be activated by lung cancer-associated TNF-α, up-regulate MMP-13 expression and thereby augment tumor metastasis.
The present study aimed to investigate the synergistic mechanisms underlying the anti-angiogenesis gene, arresten, and the apoptosis-inducing gene, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), in order to evaluate their therapeutic potential in lung cancer.
Tumor necrosis factor-alpha (TNF-α) is an important inflammatory cytokine that plays a role in controlling the progression of lung cancer, hepatocellular cancer, breast cancer and gastric cancer.
Compared with the control, no significant association was revealed between TNF-α-308G/A (GG + GC vs. CC: OR = 1.10, 95% CI: 0.73 to 1.64; GG vs. GC + CC: OR = 1.02, 95% CI: 0.81 to 1.27; GC vs. CC: OR = 1.13, 95% CI: 0.73 to 1.77; GG vs. CC: OR = 1.04, 95% CI: 0.80 to 1.36; G vs. C: OR = 1.03, 95% CI: 0.90 to 1.18) or IL-6 174G/C (GG + GC vs. CC: OR = 1.10, 95% CI: 0.73 to 1.64; GG vs. GC + CC: OR = 1.02, 95% CI: 0.81 to 1.27; GC vs. CC: OR = 1.13, 95% CI: 0.73 to 1.77; GG vs. CC: OR = 1.04, 95% CI: 0.80 to 1.36; G vs. C: OR = 1.03, 95% CI: 0.90 to 1.18) and lung cancer risk.
We previously prepared a TNF mutant (rmhTNF) that significantly improved responses in lung cancer patients and exhibited a promising safety profile in phase I and II studies.
Interestingly, PHLPP2 expression was inversely associated with tumor necrosis factor alpha (TNFα) expression, with low PHLPP2 and high TNFα expression in lung cancer tissues compared with the paired adjacent normal lung tissues.
The meta-analysis suggests that TNF-α gene 308G>A polymorphism is associated with an increased risk of lung cancer, particularly among Asians, both for SCLC and NSCLC, considering tumor type.
As TNFA triggers a cytokine cascade, the modifying effect of the TNFArs1799724 genotypes on the association of any of the remaining polymorphisms with lung cancer risk was also examined.
In the study, we designed to investigate the effect of TNF-α on the activation and expression of nuclear factor kappa B (NF-κB)/p65/SLUG/PUMA/Bcl-2 levels in human lung cancer A549 cell line, and in conditions of TNF-α-induced apoptosis.
Resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a prerequisite for cancer progression, and TRAIL resistance is prevalent in lung cancer.
We found that the TNF-α and IL-6 polymorphisms may be a critical risk for the genetic susceptibility to lung cancers in the ethnic group Han of North China.
We therefore investigated the systemic delivery of tumor necrosis factor-related apoptosis-inducing ligand-expressing oncolytic Ad genome DNA (pmT-d19/stTR) via lipid envelopment as an alternative approach for cancer virotherapy in an orthotopic lung cancer model.
Bayesian correction for multiple comparisons suggests that chance is unlikely to explain our findings (although epigenetic mechanisms may be in effect), which support our hypotheses, suggesting that IL10 rs1800871 is a susceptibility marker for oropharyngeal and lung cancers, and that TNFrs1799964 is associated with smoking-related cancers among never smokers.
We show here that the TG2 inhibitor KCC009 reversed resistance to tumor necrosis factor-related apoptosis-inducing factor (TRAIL) in lung cancer cells.
4EGI-1, as a single agent, inhibited the growth and induced apoptosis of human lung cancer cells.When combined with the death ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), enhanced apoptosis-induced activity was observed.
The present study investigated whether the TNF-alpha-308 and TNF-alpha-238 polymorphisms are associated with risk and/or severity of disease in Croatian lung cancer patients.