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-6174G/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.
Additionally, we found that an IL8 promoter polymorphism had a protective effect for lung cancer in female subjects, whereas an IL6 promoter polymorphism was only associated with risk of squamous cell carcinoma.
Single nucleotide polymorphisms (SNPs) in IL-6, IL6-R, and IL6-ST genes were assessed in 120 controls and 120 patients with confirmed lung cancer diagnosis.
The influence of tumor necrosis factor-alpha -308 G/A and IL-6-174 G/C on pain and analgesia response in lung cancer patients receiving supportive care.
Higher level of interleukin-6 (IL-6) existed in lung cancer patients and mutant EGFR and TGFβ signal requires the upregulation of IL-6 through the gp130/JAK pathway to overactive STAT3, an oncogenic protein which has been considered as a potential target for cancer therapy.
Our results suggest that BSF2 polymorphism may not predispose genetic susceptibility toward lung cancer in Caucasian populations, which nevertheless requires additional investigation.
The IL-6 -174C allele showed a tendency towards a higher risk for fibrosis or asbestos-induced lung cancer (ORasbestosis, 1.338; 95% CI, 0.71-2.53; ORsilicosis, 1.226; 95% CI, 0.54-2.81; ORfibrosis other aetiology, 1.313; 95% CI, 0.58-2.98 and ORLC asbestos, 2.112; 95% CI, 0.75-5.92).
The present meta-analysis suggested that there was no association between IL-6rs1800796 polymorphism and lung cancer, which was independent of smoking status.
We assessed whether single nucleotide polymorphisms (SNPs) in the IL6 promoter are associated with lung cancer in former uranium miners with high occupational exposure to radon gas.
Taken together, these results indicate that IL-6 deletion accelerates tumorigenesis but delays tumor progression and prolongs survival time in a Kras-driven mouse model of lung cancer.
Accumulating evidence has suggested that TERT could modulate the expression of numerous genes including interleukin 6 (IL-6), an important cytokine for the development of lung cancer.
Collectively, these preclinical findings identify trans-signalling via STAT3 as the signalling modality by which IL-6 promotes muscle wasting in lung cancer cachexia, and therefore support the clinical evaluation of the IL-6 trans-signalling/STAT3 axis as a therapeutic target in advanced lung cancer patients presenting with cachexia.
The signaling pathways of interleukin-6 (IL-6) and insulin-like growth factor 1 (IGF-1) play an important role in the progression of lung cancer, and this study aimed to explore whether they can synergistically promote the progression of non-small cell lung cancer (NSCLC).