co-stimulatory mechanisms may exist that increase the expression of cox-2 and laminin-5 at the invasive front of lung adenocarcinomas and that EGFR signaling could be one of the mechanisms

greater expression seen in adenocarcinoma rather than squamous cell carcinoma of lung; no correlation seen between increased expression and major clinicopathologic factors

increased expression associated with development of lung cancer and possibly acquisition of invasive/metastatis phenotype

Autocrine/paracrine prostaglandin E2 production by non-small cell lung cancer cells regulates matrix metalloproteinase-2 and CD44 in enzyme-dependent invasion

Abnormal interleukin 10Ralpha expression contributes to the maintenance of elevated cyclooxygenase-2 in non-small cell lung cancer cells.

In this study, we have used quantitative PCR to analyse expression of beta-tubulin III, stathmin, RRM1, COX-2 and GSTP1 in mRNA isolated from paraffin-embedded tumor biopsies of 75 nonsmall-cell lung cancer patients treated as part of a randomized trial

Stabilization of survivin may contribute to the apoptosis resistance effect of COX-2 in non-small cell lung cancer.

Cyclooxygenase 2 gene polymorphism is associated with non-small cell lung cancer.

COX-2 up-regulates VEGF-C and promotes lymphangiogenesis in human lung adenocarcinoma via the EP(1)/Src/HER-2/Neu signaling pathway.

Fibronectin stimulates human lung carcinoma cell proliferation and diminishes apoptosis by inducing COX-2 gene expression and PGE2 biosynthesis.

Review of COX-2 in lung cancer treatment. COX-2 plays a role in lung cancer and may be a marker of prognosis.

COX-2 expression in both cancer cells and stromal cells within the lung cancer microenvironment may play an important role in upregulating the expression of the angiogenic factor VEGF in lung cancer.

the COX-2 T8473C polymorphism may contribute to lung cancer susceptibility in the Chinese population

Significantly higher expression of cyclooxygenase 2 is associated with metastasis in non-small cell lung cancer

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

the COX-2 8473T>C polymorphism may have a role in development of adenocarcinoma of the lung

This effect is statistically significant in lung cancer stage I, suggesting that COX-2 expression could be useful at early stages to distinguish those with a worse prognosis.

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

epiregulin, COX2, and MMP1 and 2 collectively facilitate the assembly of new tumour blood vessels, the release of tumour cells into the circulation, and the breaching of lung capillaries by circulating tumour cells to seed pulmonary metastasis

Signaling pathways involved in PTGS2 induction by hepatocyte growth factor in non-small-cell lung carcinoma are reported.

Results show co-expression of cyclooxygenase-2 and prostaglandin E2 receptors EP1, 2 and 4 in non-small cell lung cancer cells concomitant with the synthesis of PGE2.

COX-2 (-1195G) is likely to result in a better non-small cell lung cancer response to vinorelbine (nonsignificant).

Wogonin inhibits phorbol myristatae acetate-induced COX-2 gene expression in a lung cancer cell line.

Results indicate that the pro-tumorigenic function of Angiotensin II is attributable, in part, to its strong stimulatory effect of COX-2 expression in lung fibroblasts in which synergistic stimulation with pro-inflammatory cytokines was evident.

Report role of p53 in the induction of cyclooxygenase-2 by cisplatin or paclitaxel in non-small cell lung cancer cell lines.

On the basis of the results obtained the use of exhaled breath condensate COX-2 and survivin levels could be suggested as two potential markers within an early non-invasive screening of populations of smokers at risk of lung cancer.

This meta-analysis suggests that -765G>C may cause an increased risk of colorectal carcinoma and esophageal cancer in Asian descents while 8473T>C polymorphism may cause a decreased risk of breast and lung cancer.

Single nucleotide polymorphisms in PTGS2 gene is associated with non-small cell lung cancer.

Results provide evidence that the A allele of Cox-2 intron 6 may be associated with the development of lung cancer and may be a useful marker for early detection and treatment of lung cancer.

Co-overexpression of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 is associated with postoperative non-small cell lung cancer.

the COX-2-765G-->C and -1195A-->G genotypes may be a risk factor for lung carcinoma

Overexpression of EGFR and COX-2 may play an important role in the tumorgenesis, progression and malignancy of lung cancer. Detection of EGFR and COX-2 expression might be helpful to diagnosis and prognosis of lung cancer.

The expression of COX-2 was significantly associated with the expressions of transcription factors NFAT3 and c-Fos in nonsmall cell lung cancer.

results suggest the COX-2 gene is a factor for suffering from lung cancer, especially of small cell type among Asians

COX-2 and EGFR are overexpressed in non-small cell lung cancer.

The expression of COX-2 in squamous cell carcinomas carcinomas could be a useful independent prognostic marker in lung neoplasms.

Single nucleotide polymorphism in PTGS2 is associated with low-stage non-small cell lung cancer.

COX-2 mRNA levels were higher in the lung parenchyma of COPD patients than in controls. COX-2 protein (but not mRNA) levels were higher in adenocarcinoma than in squamous carcinoma. COX-2 may be involved in the association between COPD & cancer.

Meta-analysis suggests that the COX 2 T8473C polymorphism is not associated with lung cancer risk.

single nucleotide polymorphisms within the PTGS2 and LTA inflammatory markers were associated with pain and quality of life in a large sample of long term lung cancer survivors

Higher levels of PTGS2 is associated with the formation of an M2-macrophage-dominant tumor microenvironment in lung cancer.

Data show that p38 MAPK, ERK1/2, and COX-2 activation are mediators for the galectin-1-promoted tumor progression and chemoresistance in lung cancer.

a potentially synergistic association of PTGS2 and CYP2E1 polymorphisms with the underlying cause of lung cancer in northeastern Chinese

This investigation for the first time suggested that polymorphism in COX-2 rs689466 may be a potent bio-marker in predicting severe hematologic toxicity in non-small-cell lung cancer patients after platinum-based chemotherapy.

Gene knockdown of COX-2 by lentivirus-COX-2-siRNA significantly inhibited the growth and induced cell cycle arrest of non-small lung cancer cell lines.

Upregulation of COX-2 in lung cancer promotes overexpression of multidrug resistance protein 4 via PGE2-dependent pathway

Decreased miR-146a expression contributes to the up-regulation and overexpression of COX-2 in lung cancer cells.

PTGS2 overexpression and -8473 T/C polymorphism in 3' UTR are associated with non-small cell lung cancer.

The COX-2 -1195G/A polymorphism influences the infiltration of Tregs into non-small cell lung cancer.

High COX2 expression is associated with lung adenocarcinoma and squamous cell carcinoma.

Low stromal expression of COX-2 is associated with adenocarcinoma in non-small cell lung cancer.

High Cox-2 expression is associated with poor response to platinum-based chemotherapy in non-small cell lung cancer.

Results indicate that VEGFR2 -906, COX-2 -1195 and MMP-2 -1306 variants and their combinations may signi fi cantly in fl uence clinical outcome in inoperable non-small cell lung cancer patients treated with radiotherapy with or without chemotherapy.

11betaHSD2 inhibition suppressed lung tumor growth and invasion in association with increased tissue active glucocorticoid levels, decreased COX-2 expression, inhibition of ERK and mTOR signaling pathways.

AA genotype of COX-2 rs689466 and CC genotype of COX-2 rs5275 still contributed to increased risk of non-small cell lung cancer

Findings suggest that COX-2 deletion contributes to the repression of K-ras-induced lung tumorigenesis by reducing tumor cell proliferation, decreasing the production of PGE2, and increasing the production of 13,14-dihydro-15-keto-PGE2, possibly via the MAPK pathway.

results demonstrate that hnRNPA2/B1 promotes tumor cell growth by activating COX-2 signaling in NSCLC cells and imply that the hnRNPA2/B1/COX-2 pathway may be a potential therapeutic target for human lung cancers.

Cleavage and polyadenylation specific factor 4 targets NF-kappaB/cyclooxygenase-2 signaling to promote the growth and survival of non-small cell lung carcinoma cells.

Bisphenol A (BPA) induced COX-2 expression via nuclear translocation of NF-kappaB and activation of mitogen-activated protein kinase (MAPK) by phosphorylation of ERK1/2 and enhanced the migration of lung cancer A549 and breast cancer MDAMB-231 cells.

meta-analysis demonstrated that COX-2 rs5275 and rs689466 polymorphism significantly decrease the risk of lung cancer in Asians but not in Caucasians, indicating COX-2 could serve as a potential diagnostic marker for lung cancer

cyclooxygenase-2 and iNOS, two inflammation related enzymes, playing important roles in the carcinogenesis of 3-methylcholanthrene and diethylinitrosamine, induce rat lung squamous cell carcinoma as well as its metastasis.

COX-2 may play an important role during the carcinogenesis in experimental rat lung squamous cell carcinoma as well as its metastasis, partly by stimulating angiogenesis

Cyclooxygenase-2 expression influences the growth of human large and small cell lung carcinoma lines in athymic mice: impact of an organoselenium compound on growth regulation

C/EBP and ATF/CREB as the major transcriptional regulators of basal expression of COX-2 in these lung tumor-derived cell lines

Arginase I in myeloid suppressor cells is induced by COX-2 in lung carcinoma.

These results suggest a crucial role for the COX-2 signaling pathway in the intermittent hypoxia-exacerbated malignant processes, and designate macrophages and lung adenocarcinoma cells, as potential sources of prostaglandin E2.