Nuclear factor-kappa b knockdown exerts anti-inflammatory effects on LPS-induced acute lung injury especially in the initial phase, which may be due in part to reduced levels of the proinflammatory cytokine tumor necrosis factor alpha.

NF-kappaB plays a key role in the resistance of lung cancer cells to TNF and TRAIL

a common mediator of inflammation can lead to the induction of SSAT expression by activating the NFkappaB signaling pathway in non-small cell lung cancer cells

COX-2 is downregulated by PC-SPES via inhibition of NF-kappaB and C/EBPbeta in non-small cell lung cancer cells

using bioluminescent detection of NF-kappaB activation in mouse lug adenocarcinoma cells, we found a negative impact of p65/RelA on non-small cell lung cancer metastasis

that Adriamycin-induced NF-kappaB is a transcriptional activator that protects lung cancer cells against apoptosis

Cytoplasmic apurinic endonuclease 1 could enhance lung tumor malignancy through NF-kappaB activation.

Apoptosis induced in lung cancer cells by the thromboxane synthase inhibitor 1-benzylimidazole is associated with the over-production of ROS and the reduction of NF-kappaB.

NF-kappaB targeting by way of IKK inhibition sensitizes lung cancer cells to adenovirus delivery of TRAIL

the expression of miR-9 and let-7g could enhance the efficiency of radiotherapy for lung cancer treatment through the inhibition of NFkappaB1.

deregulation of the alternative NF-kappaB pathway in non-small cell lung cancer could play a role in the development and progression of the disease

Data show that hypoxia upregulates the expression of Annexin A1 in lung adenocarcinoma A549 cells, in which process reactive oxygen species (ROS)-NF-kappaB may paticipate in.

A significant association was observed between a variant in the NFKB1 gene and the risk of lung cancer.

a common susceptible mechanism of inflammation in lung induced by genetic variants in NFkappaB1 (-94del>ins ATTG) or IkappaBalpha (2758G>A) to predict risk of COPD or lung cancer.

According to the results, the NF-kappaB1-94ins/del ATTG promoter polymorphism may have a role in lung carcinogenesis and prognosis.

FACT, NF-kappaB, and cell-cycle progression are inhibited by quinacrine, which overcomes resistance to erlotinib in non-small cell lung cancer

Trim44 promotes non-small cell lung cancer development through activation of NF-kappaB signaling via upregulating CXCL16 and MMP9 expression.

Data suggest that the status of p53 and KRAS may be considered for the targeted therapy against NF-kappaappa B in lung cancer patients.

knockdown of PTX3 suppressed tumor proliferation and invasion of lung adenocarcinoma cells, followed by decreased expression of p-AKT, p-NF-kappa B, PCNA, and MMP-9

results suggest that NFKB1 common variants and smoking duration and smoking duration-PPP1R13L rs1970764 interaction could be concerned with the lung cancer development in a Chinese population

In non-small cell lung cancer, P50 was predominantly expressed in intratumoral stroma. tumor P50 was an independent predictor of TNM6 stage IIB or higher.

we were able to reproduce previously found associations between PPP1R13L and CD3EAP polymorphisms and lung cancer risk in an increased study group, and we found interactions between NFKB1 rs28362491-PPP1R13L rs1970764 and smoking duration and between CD3EAP rs735482 and smoking duration

This study identified HOXA9 as a target gene of miR-196b and determined that the mechanism of miR-196b-mediated epithelial-to-mesenchymal transition and invasion processes involves the regulation of HOXA9 expression in non-small cell lung cancer cells.

Data show that the effect of curcumin in decreasing the migratory and invasive ability of lung adenocarcinoma A549 cells by inhibiting adiponectin expression is probably mediated through NF-kappaB/MMP pathways

NF-kappa B activation links Chronic obstructive pulmonary disease and lung cancer through generation of an immunosuppressive microenvironment in the lungs.

Our findings indicate that FOXO3a is a significant factor in EGFR mutation-independent gefitinib resistance and the stemness of lung cancer, and suggest that targeting the NF-kappaB/miR-155/FOXO3a pathway has potential therapeutic value in lung cancer with the acquisition of resistance to EGFR-TKIs.

High NF kappa B expression is associated with lung tumorigenesis.

High NF-kappa-B expression is associated with lung cancer.

Co-expression of p65 and phosphorylated p105 but not of either p65 or phosphorylated p105 alone was associated with a poor prognosis in surgically resectable non-small cell lung cancer patients.

RNF25 plays an essential role in gefitinib resistance of Non-small cell lung cancer by mediating cross-talk between NF-kappaB and ERK pathways.

Prognostic significance of NF-kappaB expression in non-small cell lung cancer

HMGB1 promoted lung cancer invasion and metastasis by upregulating the expression and activity of MMP-2 in an NF-kappaB-dependent manner.

SPOP inhibits NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity and its target genes expression via FADD in non-small cell lung cancer

NFkappaB and TNFalpha were identified as the most significantly up-regulated molecules in cisplatin-resistant and radioresistant lung cancer cells, respectively, compared with parental cells.

Targeting the KRAS, p38alpha, and NF-kappaB in lung adenocarcinoma cancer cells has been reported.

miR379 inhibits cell proliferation and epithelialmesenchymal transition by targeting CHUK through the NFkappaB pathway in nonsmall cell lung cancer.

High NF-kB expression is associated with radio-resistance of docetaxel-resistant lung Adenocarcinoma.

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.

Inhibition of arachidonate lipoxygenase12 targets lung cancer through inhibiting EMT and suppressing RhoA and NF-kappaB activity.

The Fire Within: NF-kappaB Involvement in Non-Small Cell lung cancer.

Metastasis-Associated Protein 2 Represses NF-kappaB to Reduce lung tumor Growth and Inflammation.

persistent NF-kappaB signaling in airway epithelium facilitates carcinogenesis by sculpting the immune/inflammatory environment in the lungs

CCR5 deficiency suppressed lung tumor development through the inhibition of nuclear factor-kappaB/STAT3 pathways and the downregulation of MCP-1 in the carcinogen-induced lung tumor model.

up-regulated expression during benzo(a)pyrene induced pulmonary carcinogenesis

Results show a caspase recruitment domain-containing protein 9 (CARD9)-NF-kappa B (NF-kappaB)-IDO Dioxygenase (IDO) pathway in myeloid-derived suppressor cells (MDSCs) which can inhibit the suppressive function of MDSCs and prevent lung cancer development.