Functional prediction revealed that 8 lncRNAs have potential effects on tumor immune processes such as lymphocyte activation and TNF production in NSCLC.
Consistently, we found an increased expression of IL-35<sup>+</sup>Foxp-3<sup>+</sup> cells, which associated with ARG1 mRNA expression and decreased TNFA in the TU region of the lung of patients with NSCLC as compared to their CTR region.
The expression of IRF5 and its associated inflammatory factors IL-6, IL-10, IP-10, and TNF-α in the peripheral blood of NSCLC patients (n = 66) and healthy controls (n = 42) was analysed by quantitative RT-PCR, flow cytometry, and a cytometric bead array.
In the present study, we compared expression level of Fas-antisense 1 (FAS-AS1), Growth Arrest Specific 5 (GAS5), PVT1, Nuclear Paraspeckle Assembly Transcript 1 (NEAT1), HOXA transcript antisense RNA myeloid-specific 1 (HOTAIRM1), taurine upregulated gene 1 (TUG1) and TNFα and hnRNPL related immunoregulatory LincRNA (THRIL) in 32 NSCLC samples and their corresponding adjacent non-cancerous tissues (ANCTs).
By contrast, high expression of tumor necrosis factor receptor-associated protein 1 (TRAP1) mRNA was significantly associated with improved OS rates in all NSCLC patients combined (HR, 0.88; 95% CI: 0.77-0.99; P=0.041), as well as ADE patients.
Using assays to evaluate cell proliferation, apoptosis, and gene expression, we investigated the efficacy of MSCs expressing tumour necrosis factor (TNF)-related apoptosis inducing ligand (MSC-TRAIL) to target and destroy CD133+ (prominin-1 positive) NSCLC-derived CSCs.
We hypothesize that single nucleotide polymorphisms (SNPs) in the TNF/TNFR pathway genes related to apoptosis are associated with survival of patients with non-small cell lung cancer (NSCLC).
The current study has demonstrated that osimertinib reduces c-FLIP levels via facilitating its degradation and enhances apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) primarily in NSCLC with activating EGFR mutations.
Here we investigated the different susceptibility of glutamine-independent and glutamine-dependent non-small cell lung cancer (NSCLC) to treatment with tumor necrosis factor receptor-associated protein 1 (TRAP1) inhibitor gamitrinib-triphenylphosphonium (G-TPP).
We report here that DDIAS protects cancer cells from tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by two distinct mechanisms in non-small cell lung cancer (NSCLC) and hepatocellular carcinoma (HCC) cells.
The aim of this study was to evaluate potential prognostic and predictive biomarkers interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α) and a panel of interleukins (ILs) in the peripheral blood, and assess any correlation with response to anti-PD-1 inhibition, progression-free survival and OS in NSCLC patients.
IFNγ/AZD5582-induced cell death in NSCLC cells was independent of TNFα autocrine but relied on apoptosis mediated by JAK kinase, caspase 8 and RIPK1 pathways.
The mechanism underlying increased concentrations of cancer stem cell (CSC)-associated factors in non-small cell lung cancer (NSCLC) cells treated with transforming growth factor β1 (TGFβ1) and tumor necrosis factor α (TNFα), is still not clear.
As a cytokine belonging to the Tumor Necrosis Factor-α (TNF- α) family, the - a proliferation-inducing ligand (APRIL) expression and its signaling have been studied in many human solid tumor types, but the data on APRIL signaling in NSCLC are lacking.
The case-controlled cross-sectional study design recruited 77 patients with confirmed diagnosis of NSCLC (cases) and 91 healthy subjects (controls) aimed to examine peripheral pro-inflammatory and anti-inflammatory cytokines (IL-2, IL-4, IL-6, IL-10, IL-17A, TNF and IFN-γ) by Cytometry Beads Arrays (CBA Flex) in.
We investigated the mast cell phenotype in terms of protease content (tryptase-only [MC<sub>T</sub>], tryptase + chymase [MC<sub>TC</sub>]) and tumour necrosis factor-alpha (TNFα) expression, and extent of degranulation, in NSCLC tumour stroma and islets.
Here, we aimed at establishing a suitable treatment regimen for the multi-target TKI sunitinib and the tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in NSCLC-derived cells with or without EGFR and KRAS mutations.