Interleukin-6 is an important independent mediator of elevated C-reactive protein concentrations in patients with non-small-cell lung cancer.

IL-10, but not TNF-alpha, TNF-beta, or IL-6 polymorphisms are associated with lung cancer

Cyclooxygenase-2-dependent activation of STAT3 by interleukin-6 has a role in non-small cell lung cancer

These results suggest that IL-10, TNF-alpha and TGF-beta1 gene polymorphisms may affect host susceptibility to lung cancer and the outcome of the patients.

EGFR could activate the gp130/JAK/STAT3 pathway by means of IL-6 upregulation in primary human lung adenocarcinomas, making this pathway a potential target for cancer treatment.

HPV 16/18 up-regulates the expression of interleukin-6 and antiapoptotic Mcl-1 in non-small cell lung cancer

analysis of the role of IL-6 and VEGF in small cell lung cancer

The higher the serum IL-6 levels on postoperative day 1, the higher the risk of early postoperative recurrence, even when curative pulmonary resection can be accomplished in lung cancer patients.

Review: Report role of humanized anti-IL-6 antibody (ALD518) in non-small cell lung cancer.

AhR, without exposure to a ligand, associates with RelA, which then positively modulates NFkappaB activity and then upregulates IL-6 expression in human lung cells; a new mechanism for lung tumorigenesis

The expression of IL-6 in tumor correlated with the concentration of serum IL-6, tumor progression, and overall survival in patients with non-small-cell lung cancer

High serum IL6 is associated with advanced nonsmall cell lung cancer.

This is the first evidence of identifying an IL-6 promoter haplotype (CC) associated with increased risk of lung cancer.

Single-base changes in the TNFA and IL6 alleles correlated with occurrance of lung cancers in the Han ethnic group.

High serum IL6 levels are associated with advanced stages of non-small cell lung cancer.

meta-analysis suggested that IL6 -634C/G polymorphism was a risk factor for lung cancer

TERT rs2736100T/G polymorphism modulates IL-6 expression and may play a unique role in lung adenocarcinoma.

No significant publication bias was observed. In conclusion, we found that -634C>G and -174G>C polymorphisms in IL6 promoter region were not associated with lung cancer risk

Data indicate that metformin reverses epithelial-mesenchymal transition and decreases interleukin-6 signaling in EGFR-TKI-resistant lung cancer cells.

Il-6, IL-17, TNF-alpha and VEGF levels were measured in exhaled breath condensate and serum of 15 patients with stage I-IIA non-small cell lung cancer.

suggest that targeting of the IL-6/JAK2/STAT3 signaling pathway and DNMT1 may become important strategies for treating lung cancer

The present meta-analysis suggested that there was no association between IL-6 rs1800796 polymorphism and lung cancer

lung cancer cells upregulate IL-6 secretion by activating the p38/NF-kappaB pathway through treatment with cisplatin and camptothecin.

Our clinical and experimental studies revealed that serum IL-6 is a surrogate marker for evaluating cachexia and the prognosis of patients with chemotherapy resistant metastatic lung cancer

BSF2 polymorphism did not play a major role in the progression of lung cancer.

relationship between IL-6-643 (C/G) and IL-1beta-31 (C/T) polymorphisms and lung cancer risk among female non-smokers

signalings can reciprocally and positively regulate each other, leading to enhanced non-small cell lung cancer (NSCLC) cell proliferation and survival.

The main finding of our meta-analysis reveals that increased serum IL-6 levels may contribute to the incidence of radiation pneumonitis in lung cancer patients, especially among Caucasians.

IL-6 gene -174G>C polymorphism was not associated with lung cancer.

IL-6 signaling has a role in cisplatin resistance in non-small cell lung cancer via the up-regulation of anti-apoptotic and DNA repair associated molecules

An IL6 promoter variant was associated with lung cancer in uranium miners and never smokers in two external study populations. The associations are strongly supported by the functional relevance that the IL6 promoter SNP affects basal expression and carcinogen-induced IL-6 secretion.

High IL-6 promotes growth and epithelial-mesenchymal transition of CD133+ cells of non-small cell lung cancer.

Ninj1 suppresses migration, invasion and metastasis of lung cancer via inhibition of the IL-6 signaling pathway in vitro and in vivo.

we evaluated anti-IL-6 receptor antibody treatment of cancer-related anemia in an IL-6-producing human lung cancer xenograft model.We demonstrated that inhibition of the IL-6 signaling pathway by MR16-1 treatment resulted in significant recovery of iron-deficiency anemia and alleviation of cancer-related symptoms

IL6 overexpression is associated with lung cancer.

the sensitivity and specificity of CEA, CA125, and ProGRP when used in combination with IL-6, IL-10, and MCP in lung cancer diagnosis, was examined.

IL-6 Mediates Macrophage Infiltration after Irradiation via Up-regulation of CCL2/CCL5 in Non-small Cell lung cancer

Studied the tumor suppressive role and antiproliferative effect of MicroRNA-218 in lung cancer cells through targeting of IL-6/STAT3 pathway.

Study revealed that IL-6, which was expressed in the lung induced cancer stem cells (CSCs), facilitates the formation of lung cancer organoids via the conversion of mesenchymal stem cells into alpha-SMA-positive cells. Furthermore, IL-6 mRNA-positive cancer cells were found in clinical lung cancer samples.

The combination of EGFR-TKI and anti-IL-6 antibody moderately improved the sensitivity of EGFR-TKI in lung cancer cell with EGFR mutation. Interestingly, suppression of EGFR with EGFR-TKI accelerated the activation of STAT3 induced by IL-6. Taken together, tumour IL-6 levels might indicate a subpopulation of EGFR-mutant NSCLC that benefits less from gefitinib monotherapy.

IL6 expression is regulated by miR-26a in ambient particulate matter-bound metal-triggered lung cancer.

Results show that IL-6 expression increases in osteosarcoma (OS) primary tumor cells and in metastasized lung tumor. The increased IL-6 expression is mediated by TET2- dependent demethylation activity in OS cells and links the hypoxic tumor microenvironment to acquisition of aggressive tumor cell phenotypes.

IL-11, an IL-6 Family Cytokine, promotes Non-Small Cell lung cancer cell proliferation in vitro and tumorigenesis in vivo.

Our results showed that IL-37 plays an inhibitory role in non-small cell lung cancer progression, possibly by suppressing STAT3 activation and decreasing epithelial-to-mesenchymal transition by inhibiting IL-6 expression. IL-37 could serve as a potential novel tumor suppressor in non-small cell lung cancer

data showed that activation of NF-kappaB/IL-6 is involved in estrogen-related receptor alpha induced migration and invasion of non-small cell lung cancer cells; it suggested that ERRalpha might be a potential target for non-small cell lung cancer treatment

the combined detection of IL-6 and tumour markers is critical to improve the specificity and sensitivity of lung cancer diagnosis. This in-depth study not only helped to elucidate the mechanism of how IL-6 promotes lung cancer but also provided new ideas and entry points to resolve the low specificity and sensitivity of lung cancer-related tumour markers.

Study found that IL-6, GP130, IGF-1 and IGF-1R were highly expressed in non-small cell lung cancer (NSCLC) and there was the correlation between GP130, IGF-1, and IGF-1R. Co-stimulation of IL-6 and IGF-1 resulted in significantly enhanced cell proliferation, invasion, and apoptosis of NSCLC cells. This experiment revealed that IL-6 and IGF-1 can synergistically promote the progression of NSCLC.

These findings support that there is a direct correlation between cytokines including interleukin-6, interleukin-8, interleukin-10, and tumor necrosis factor-alpha and cardiopulmonary bypass time, duration of operation, and intensive care unit stay.

we found that lung cancer cells induced Adipose-derived mesenchymal stem cells (ADSCs) to secrete high levels of IL-6 family cytokines and activate the STAT3 signalling pathway.

The IL-6 (rs2069840) polymorphism may influence the occurrence of lung cancer in Moroccan patients.

Reciprocal regulation of miR-206 and IL-6/STAT3 pathway mediates IL6-induced gefitinib resistance in EGFR-mutant lung cancer cells.

IL-6 in tumour microenvironment enhances TIM-4 expression in lung cancer cells via NF-kappaB, which in turn promotes metastasis and IL-6 production of lung cancer cells.

IL-6 stimulates lncRNA ZEB2-AS1 to aggravate the progression of non-small cell lung cancer through activating STAT1.

Effects of sevoflurane inhalation anesthesia on IL-6, TNF-alpha and MMP-9 expression and hemodynamics in elderly patients undergoing lobectomy for lung cancer.

Loss of Interleukin 6 is associated with lung carcinogenesis.

Early production of IL-6 in the pulmonary microenvironment is followed by autocrine secretion of IL-6 by the tumor cells. This plays an important role in optimal tumor growth, leading to activation of MAPK & STAT3 signaling.

Mesenchymal stem cells enhance lung cancer initiation through activation of IL-6/JAK2/STAT3 pathway.

Loss of p53 attenuates the contribution of IL-6 deletion on suppressed tumor progression and extended survival in Kras-driven murine lung cancer.

Data indicate a role of interleukin 6 (IL6)/transcription factor STAT3 (STAT3) signaling in maintaining lung homeostasis and suppressing lung cancer induction.

Adipose-derived stem cells play a pro-malignant role in tumor development of Lewis lung carcinoma cells by particularly promoting cancer stem cell property through interleukin-6 paracrine circuit.

Lewis lung carcinoma cell-derived extracellular vesicles induced myotube atrophy and adipocyte lipolysis via the extracellular IL-6-mediated STAT3 pathway in target cells.