expression of membrane-type-1-matrix metalloproteinase and metalloproteinase-2 in nonsmall cell lung carcinomas

Autocrine/paracrine prostaglandin E2 production by non-small cell lung cancer cells regulates enzyme and cd44 in cox-2-dependent invasion

Various growth factors induce migration of human non-small cell lung cancer cells in the presence of extracellular matrix (ECM) components MMP-2 and MMP-9.

Overexpression of MMP-2 is associated with non-small cell lung cancer

the -735C/T MMP-2 polymorphism might be an independent prognostic marker in non-small cell lung cancers

Elevated activities of MMP-2 in the non-tumorous lung tissues of curatively resected stage I NSCLC patients are associated with tumor recurrence

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

results suggest that MMP2 is a more sensitive predictor than MMP9 of lung cancer progression, metastasis, and survival

Crucial participants in tumour invasion and metastases are matrix metalloproteinases, tissue inhibitor of metalloproteinase inhibitors and cellular adhesion molecules. They play roles in tumour invasion and metastasis in non-small-cell lung carcinomas.

Data suggest that Fra-1 enhances lung cancer epithelial cell motility and invasion by inducing the activity of matrix metalloproteinases, in particular MMP-2 and MMP-9, and EGFR-activated signaling.

MMP-2 is valuable in determining the patients with more aggressive form of non-small cell lung cancer..

curcumin has anti-metastatic potential resulting in inhibition of MMP-2 and -9 in human lung cancer A549 cells.

The MMP-2 polymorphism was significantly associated with protection against lung cancer.

Up-regulation of MMP-2 and MMP-9 is one of the mechanisms by which Skp2 promotes lung cancer cell invasion.

SNPs in MMP1, MMP2, MMP7 and MMP12 have roles in response to chemotherapy in lung cancer

expression of MMP-2 and TIMP-1 was found to be higher in lung cancer patients. Finally, we claim that determination of MMP-9 enzyme levels and expression of MMP-2 and -9 and TIMP-1 can be used as a marker in lung cancer.

cytokines and inhibitors have an up- or down-regulatory effect on MMP-2 and MMP-9 expression in lung cancer and malignant mesothelioma

Findings suggest an important role for MMP-2 in transformation mediated by HMGA1 in large-cell, undifferentiated lung carcinoma and support the development of strategies to target this pathway in selected tumors.

ICAM-3 enhances the migratory and invasive potential of human non-small cell lung cancer cells by inducing MMP-2 and MMP-9 via Akt and CREB

MMP2 promoter polymorphisms was associated with lower susceptibility to lung cancer

Systematic review/meta-analysis suggesting that MMP-2 expression is of poor prognostic significance for survival in patients with non-small cell lung cancer.

The association of polymorphism frequencies of MMP-2 C1306T and MMP-2 plasma enzyme activity in lung cancer patients, was investigated.

tumor MMP-2 high expression was not significantly correlated with poorer outcome in stage IA non-small cell lung cancer.

fibulin-3 negatively modulates the invasiveness of lung cancer cells via regulation of MMP-7 and MMP-2 and its expression is regulated by hypermethylation of the promoter region

CD147 and MMP-2 expression is correlated with the invasion and metastasis of squamous cell carcinoma and adenocarcinoma of the lungs

The MMP2 -735 T/T genotype was statistically significantly associated with a decreased survival in non-small cell lung cancer (NSCLC)

These results suggested that the inhibition on proMMP-2 expression by Liquiritigenin may be through suppression on PI3K/Akt signaling pathway, which in turn led to the inhibition of lung adenocarcinoma A549 cells migration.

currently available evidence supports the conclusion that MMP-2 C735T and C1306T polymorphisms influence susceptibility to lung cancer in Asians

We conclude that MnSOD may promote tumor aggressiveness via upregulation of the FoxM1-MMP2 axis, and that MnSOD expression can independently predict survival and relapse in patients with resected lung adenocarcinoma.

our study suggests that evaluation of beta-catenin and MMP-2 expression may have potential in diagnosis and progression in patients with non-small cell lung cancer.

Derlin-1 is overexpressed in non-small cell lung cancer and promotes invasion by EGFR-ERK-mediated up-regulation of MMP-2 and MMP-9.

MMP2-1306 C/T polymorphism decreased lung cancer risk in Asians.

expression correlates with clinical stage in non-small cell lung cancer

HPV 16 E6 up-regulates pro-angiogenic MMP-2 and MMP-9 through inducing IL-8 expression in lung cancer cells.

Decreases in the MMP-2 (-735) polymorphism GG genotype and increases in the MMP-13 (A77G) polymorphism AG and GG genotypes increase the risk for lung cancer.

Tomatidine inhibits invasion of human lung adenocarcinoma cell A549 by reducing matrix metalloproteinases expression.

The PAK5-Egr1-MMP2 signaling pathway is a critical regulator of cell migration and invasion in lung cancer cells.

miR-29c serves as a tumor metastasis suppressor, which suppresses lung cancer cell adhesion to ECM and metastasis by directly inhibiting integrin beta1 and MMP2 expression

POU5F1 enhances the invasiveness of cancer stem-like cells in lung adenocarcinoma by upregulation of MMP-2 expression.

Serum and to a larger extent sputum MMP-2 appear to be potential noninvasive markers for detecting lung cancer.

Evaluation of the microvessel density and the expression of MMP2 and MMP9 and TTF1 in the different subtypes of lung adenocarcinoma in Tunisia

These results suggested that PFIO could suppress the invasion and migration of human lung carcinoma by reducing the expression levels and activity of MMP-2 and MMP-9 via suppression of MAPKs, PI3K/AKT, and NF-kappaB signaling pathways.

LOX may play a role in the metastasis of non-small cell lung cancer by promoting MMP2/MMP9 expression.

High MMP2 expression is associated with lung cancer.

Capn4 promotes non-small cell lung cancer progression via upregulation of matrix metalloproteinase 2.

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.

data on the stromal macrophages immunoreactivity of uPAR, MMP-2, and MMP-9 in a few small cell lung cancer (SCLC) and lung squamous cell carcinoma (SCC) biopsies was included. uPAR, MMP-2, and MMP-9 were confirmed in stromal cells including macrophages

The results suggest that AQP1 may facilitate lung cancer cell proliferation and migration in an MMP-2 and-9-dependent manner.

GABRA3 induced MMP-2 and MMP-9 expression through activation of the JNK/AP-1 signaling pathway, promoting lymphatic metastasis in lung adenocarcinoma.

Data suggest that plasma levels of visfatin are up-regulated in patients with non-small cell lung cancer (NSCLC) as compared to controls; high plasma levels of visfatin correlate with neoplasm stage, lymph node metastasis, and distant metastasis; in vitro, visfatin triggers migration and invasion of NSCLC cells via up-regulation of matrix metalloproteinases 2/9 (MMP2 and MMP9).

Data suggest that MMP2 expression in lung neoplasms can be regulated by dietary factors; here, metabolites of quercetin (an antioxidant, anticarcinogenic dietary supplement) quercetin-3-glucuronide and quercetin 3'-sulfate down-regulates expression of MMP2 in A549 cells; the mechanism for this enzyme repression appears to involve up-regulation of PPARgamma.

Overexpression of MMP2 and EGFR were independent risk factors for mortality in non-small cell lung cancer patients.

The results of our pilot study indicated the diagnostic potential of miR-29b and MMP-2, an inverse association between miR-26a and MMP-2, and proved the role of MMP-2 and miR-26a, miR-29b and miR-519d in lung carcinogenesis

overexpression of LATS2 resulted in mobility inhibition in non-small cell lung cancer cell lines A549 and H1299, and reduced protein level of matrix metalloproteinase-2 (MMP-2) and MMP-9.

RNA interference (RNAi) of aquaporin 3 (AQP3) retarded the growth and invasiveness of XWLC-05 lung cancer cells and decreased the activity of matrix metalloproteinase 2 (MMP2).

MMP-2 promoted and MMP-13 disrupted vasculogenic mimicry formation in large cell lung cancer by cleaving laminin-5 to influence EGFR signal activation.

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

Data provide evidence that MMP2 expression is regulated by lnc-MMP2-2 by increasing it through its enhancer activity in lung cancer cells.

Results suggested that a reduction in CLDN18-dependent ZO-2 expression enhances MMP2 expression in lung adenocarcinoma cells, resulting in the promotion of the cell migration.

linc00858 acted as a competitive endogenous RNA to sponged miR-3182 and regulate MMP2 in lung cancer

The alteration in ATF1 expression induced a change in the epidermal growth factor receptor (EGFR) and matrix metalloproteinases (MMP)-2 expression level in the same tendency. Thus, we provided a potential new candidate for therapies against lung cancer, showing the possible mechanism underlying the invasion and migration of lung cancer cells

genotypes of MMP2-1306 may act as a biomarker in determining personal susceptibility to lung cancer in Taiwan

The long non-coding RNA MIAT/miR-139-5p/MMP2 axis regulates cell migration and invasion in non-small-cell lung cancer.

Irradiation might increase MMP2, MMP9, and VEGF expression in the tumor tissue of mice bearing Lewis lung cancer.