Inflammation in lung carcinogenesis: New targets for lung cancer chemoprevention and treatment

Lee, Jay M.; Yanagawa, Jane; Peebles, Katherine A.; Sharma, Sherven; Mao, Jenny T.; Dubinett, Steven M.

doi:10.1016/j.critrevonc.2008.01.004

Cited by 114 publications

(98 citation statements)

References 105 publications

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“…It is now widely accepted that inflammatory pathways contribute to the development and progression of cancer in general, and lung cancer, in particular (15)(16)(17). Importantly, polymorphisms in the IL-1β and IL-1β receptor antagonist genes have been associated with increased or decreased risk of non-small cell lung cancer (18,19), suggesting an important role for IL-1β-regulated genes in this disease.…”

Section: Discussionmentioning

confidence: 99%

CCAAT Enhancer Binding Protein-β Regulates Matrix Metalloproteinase-1 Expression in Interleukin-1β–Stimulated A549 Lung Carcinoma Cells

Armstrong¹,

Phelps²,

Vincenti³

2009

Molecular Cancer Research

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Matrix metalloproteinase-1 (MMP-1) is an inflammationinducible neutral protease that mediates extracellular matrix remodeling and promotes tumor invasion. In this study, we examined the activation of MMP-1 gene expression in A549 lung carcinoma cells stimulated with the inflammatory cytokine interleukin-1β (IL-1β). We found that MMP-1 mRNA levels were maximal following 16 hours of IL-1β stimulation and that this correlated with the expression of the transcription factor CCAAT enhancer-binding protein-β (CEBPB). Knockdown of CEBPB expression with short hairpin RNA abrogated the expression of MMP-1, MMP-3, and MMP-10 in IL-1β-stimulated A549 cells. An established CEBP element in the MMP-1 promoter was found to be required for basal and IL-1β-induced transcription. Electrophoresis mobility shift assays showed that CEBPB binds to this promoter element maximally 16 hours after IL-1β stimulation. DNA affinity chromatography studies showed that the LAP1, LAP2, and LIP isoforms of CEBPB bind to the IL-1β-responsive CEBPB site in the MMP-1 promoter. Exogenous expression of the LAP1 and LAP2 isoforms stimulated the MMP-1 promoter, whereas LIP had no effect. Phosphorylation of CEBPB at Thr 235 peaked at 16 hours in IL-1β-stimulated cells. The MEK inhibitor U0126 inhibited this phosphorylation and reduced MMP-1 gene induction. These studies establish CEBPB as an important mediator of metalloproteinase gene activation during inflammatory responses in lung cancer cells and highlight the different regulatory roles of CEBPB isoforms. (Mol Cancer Res 2009;7(9):1517-24)

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Section: Discussionmentioning

confidence: 99%

CCAAT Enhancer Binding Protein-β Regulates Matrix Metalloproteinase-1 Expression in Interleukin-1β–Stimulated A549 Lung Carcinoma Cells

Armstrong¹,

Phelps²,

Vincenti³

2009

Molecular Cancer Research

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“…L ung cancer is the leading cause of cancer deaths worldwide and lung adenocarcinoma is one of the predominant forms [1][2][3] . Given the well-established immunosuppressive properties of the tumour environment, strategies to reverse these events by stimulating host immune responses are of potential relevance.…”

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confidence: 99%

A role for T-bet-mediated tumour immune surveillance in anti-IL-17A treatment of lung cancer

et al. 2011

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Lung cancer is the leading cause of cancer deaths worldwide. The cytokine interleukin-17A supports tumour vascularization and growth, however, its role in lung cancer is unknown. Here we show, in the lungs of patients with lung adenocarcinoma, an increase in interleukin-17A that is inversely correlated with the expression of T-bet and correlated with the T regulatory cell transcription factor Foxp3. Local targeting of interleukin-17A in experimental lung adenocarcinoma results in a reduction in tumour load, local expansion of interferon-γ-producing CD4 + T cells and a reduction in lung CD4 + CD25 + Foxp3 + regulatory T cells. T-bet ( − / − ) mice have a significantly higher tumour load compared with wild-type mice. This is associated with the local upregulation of interleukin-23 and induction of interleukin-17A/interleukin-17R-expressing T cells infiltrating the tumour. Local anti-interleukin-17A antibody treatment partially improves the survival of T-bet ( − / − ) mice. These results suggest that local anti-interleukin-17A antibody therapy could be considered for the treatment of lung tumours.

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“…Thus, metastasis is one of hallmarks of malignant tumor and a major cause of death in cancer. 1,2) The matrix metalloproteinase (MMP) family proteins are proteolytic enzymes in extracellular matrix (ECM) that contribute to tumor invasion, angiogenesis, and metastasis. 3) Of MMP family, MMP-2 and -9 are mainly involved in the metastasis process.…”

mentioning

confidence: 99%

Anethole Exerts Antimetatstaic Activity via Inhibition of Matrix Metalloproteinase 2/9 and AKT/Mitogen-Activated Kinase/Nuclear Factor Kappa B Signaling Pathways

Choo

Rhee

Jeong

et al. 2011

Biological & Pharmaceutical Bulletin

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Anethole is known to possess anti-inflammatory and anti-tumor activities and to be a main constituent of fennel, anise, and camphor. In the present study, we evaluated anti-metastatic and apoptotic effects of anethole on highly-metastatic HT-1080 human fibrosarcoma tumor cells. Despite weak cytotoxicity against HT-1080 cells, anethole inhibited the adhesion to Matrigel and invasion of HT-1080 cells in a dose-dependent manner. Anethole was also able to down-regulate the expression of matrix metalloproteinase (MMP)-2 and -9 and up-regulate the gene expression of tissue inhibitor of metalloproteinase (TIMP)-1. The similar inhibitory effect of anethole on MMP-2 and -9 activities was confirmed by zymography assay. Furthermore, anethole significantly decreased mRNA expression of urokinase plasminogen activator (uPA), but not uPA receptor (uPAR). In addition, anethole suppressed the phosphorylation of AKT, extracellular signal-regulated kinase (ERK), p38 and nuclear transcription factor kappa B (NF-k kB) in HT-1080 cells. Taken together, our findings indicate that anethole is a potent anti-metastatic drug that functions through inhibiting MMP-2/9 and AKT/mitogen-activated protein kinase (MAPK)/NF-k kB signal transducers.

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Inflammation in lung carcinogenesis: New targets for lung cancer chemoprevention and treatment

Cited by 114 publications

References 105 publications

CCAAT Enhancer Binding Protein-β Regulates Matrix Metalloproteinase-1 Expression in Interleukin-1β–Stimulated A549 Lung Carcinoma Cells

CCAAT Enhancer Binding Protein-β Regulates Matrix Metalloproteinase-1 Expression in Interleukin-1β–Stimulated A549 Lung Carcinoma Cells

A role for T-bet-mediated tumour immune surveillance in anti-IL-17A treatment of lung cancer

Anethole Exerts Antimetatstaic Activity via Inhibition of Matrix Metalloproteinase 2/9 and AKT/Mitogen-Activated Kinase/Nuclear Factor Kappa B Signaling Pathways

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