Explored expression of MMP-9 and MDM2 in the oncogenesis of lung cancer in rats.

activity significantly higher in lung cancer cells than uninvolved lung parenchyma; may be involved in tumor progression

Block of mmp9 induction via vegfr-1 inhibition could be useful for the prevention of tumor metastasis in lung.

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.

Over expression of MMP-9 is associated with nonsmall cell lung carcinoma progression

MMP-9 is increased in tuberculous pleural effusions compared with transudates and malignant pleural effusions of lung cancer and is produced predominantly by epithelioid cells in the granulomas of tuberculous pleural tissues.

HIF-1alpha and CA IX, but not VEGF or MMP-9, may have a role in progression of surgically resected non-small cell lung cancer

the potentially functional polymorphisms MMP-9 P574R and R279Q, may have a role in occurrence and metastasis of primary lung cancer

High MMP-9 expression is associated with recurrent liver or lung tumors of colorectal cancer

MMP9 production in small-cell lung cancer cells is suppressed by CD9 and increased by its absence.

Frequent osteopontin expression is typical of, but not specific for malignant pleural mesothelioma, whereas it appears to select pulmonary adenocarcinoma cases with p65 and MMP-9 expression, suggesting a link with EGFR signalling pathways.

MMP-9 expression increased by SDF-1alpha enhances lung cancer invasiveness through the CXCR4/ERK/NF-kappaB signal transduction pathway

The K23 motifs of RECK protein can inhibit MMP-9 secretion and activity and attenuate metastasis of lung cancer cells.

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.

Matrix metallopeptidase 9 Arg279Gln and Arg668Gln polymorphisms are associated with non-small cell lung cancer.

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

Significantly higher expression of MMP-7 and MMP-9 in tumor tissue than in the surrounding tissue or in benign lung disease tissue supports the notion of an important role of these metalloproteinases in the growth of lung carcinoma

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

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

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

High matrix metallopeptidase 9 is associated with non-small cell lung cancer.

Gene expression of IL-8 and MMP-9 is related to the development of non-small cell lung cancer.

CCR7 induces lymph node metastasis of non-small cell lung cancer via upregulating MMP-9 expression.

Epidermal growth factor receptor-mediated tissue transglutaminase overexpression couples acquired tumor necrosis factor-related apoptosis-inducing ligand resistance and migration through c-FLIP and MMP-9 proteins in lung cancer cells

phenotypic expression on tumor-associated macrophages correlates with non-small lung cancer invasion and progression

The MMP-9 -1562 C>T polymorphism may decrease both the colorectal and lung cancer risk.

MMP-9 tumor cell high expression was significantly correlated with poorer outcome in stage IA non-small cell lung cancer.

Tamoxifen decreased the transcriptional expression of MMP-9 in SPC-A-1 lung adenocarcinoma cells.

Protein expression of VEGF, EGFR and MMP-9 is elevated in non-small cell lung carcinomas, correlating with progression.

polymorphism in the promoter region of the MMP9 gene is associated with the risk of the development of lung cancer.

high MMP-9 expression is associated with a poor prognosis in patients with non-small cell lung cancer

Elevated levels of CXCR4 and MMP-9 are found in small cell lung cancer tissues.

Data suggest that CD147 overexpression upregulated the protein expression of MMP-9, and strengthened the proliferation and invasive ability of lung adenocarcinoma cells.

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.

MMP9-1562 C/T polymorphism decreased lung cancer risk in Caucasians.

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.

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

ATDC upregulates MMP-9 to promote lung cancer cell invasion by activating ERK and JNK pathways.

findings suggest that ILK promotes lung cancer cell migration and invasion via NF-kappaB-mediated upregulation of MMP-9

DLK1 can promote the invasion of lung cancer cells by upregulating MMP9 expression, which depends on Notch signaling

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

High MMP9 expression is associated with non-small cell lung cancer.

Increase in MMP9 levels are associated with metastasis of non-small cell lung cancer.

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 MMP9 expression is associated with lung cancer.

miR-129, EGFR, and MMP9 appear to be promising therapeutic targets for preventing the metastasis of non-small cell lung cancer

Among patients with non-small cell lung cancer, tumor MMP-9 expression was associated with poor outcomes in those with adenocarcinoma, but not in those with squamous cell carcinoma.

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.

ADAM15 promotes lung cancer cell invasion through directly targeting MMP9 activation.

Study found that PLGF and MMP9 levels both significantly increased in the non-small cell lung cancer (NSCLC) specimens and were strongly correlated. PLGF regulated MMP9 in NSCLC cells, but not vice versa.

The MMP-9 expression in intratumoral stromal cells is associated with the clinicopathologic aggressiveness of lung cancer and is predominantly identified in tumors arising in emphysematous lungs.

VEGF and MMP-9 are overexpressed in lung adenocarcinoma tissues, and they have a synergistic effect on the invasion and metastasis of adenocarcinoma.

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).

High-level MMP9 activity is correlated with aggressive tumor behaviors and poor clinical outcomes in early-stage lung adenocarcinoma after complete resection.

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.

lung cancer patients showed significantly lower levels of serum VEGF (1.9 fold) and IL-8 (~9 fold) than COPD patients. VEGF level was significantly higher (2.6 fold) in metastatic than non-metastatic cancer patients. An increase in MMP-9 (~1.6 fold) levels was observed in lung cancer patients.

Aldolase A promotes lung cancer metastasis via PHD-mediated stabilization of HIF-1alpha and the subsequent activation of MMP9.

LncRNA-PVT1 regulates MMP9 expression in non-small cell lung cancer invasion.

Binding of miR-491-5p to MMP9 3'-UTR is disrupted by MMP9 rs1056628 A to C polymorphism, which is associated with gastric, breast, and lung cancer susceptibility in Iranian population.

MMP9 and TWIST1 were identified as more valuable biological targets for the early diagnosis and targeted therapy of lung cancer through Kaplan-Meier analysis of TCGA lung adenocarcinoma datasets.

HOXD-AS1 was upregulated in non-small cell lung carcinoma tissues and cell lines and promoted NSCLC cell proliferation, migration invasion via sponging miR-133b and regulating MMP9.

Association of MMP9-1562C/T and MMP13-77A/G Polymorphisms with Non-Small Cell lung cancer in Southern Chinese Population

The Combination of CD147 and MMP-9 Serum Levels Is Identified as Novel Chemotherapy Response Markers of Advanced Non-Small-Cell lung cancer.

Low GM1-expressing Lewis lung cancer cell lines showed increased proliferation and invasion, enrichment in the GEM/rafts, and increased secretion of MMP-9

lung tumors from MMP9-deficient mice showed decreased angiogenesis. Surprisingly, the antimetastatic outcome of MMP9 ablation seemed to be dependent on strain. Only mice that had genetic background derived from C57BL/6 showed reduced metastasis

Both MMP-9 and TIMP-1 are highly expressed in Lewis lung cancer, and are correlated to tumor invasion and metastasis.

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

MMP-9 is crucially involved in radiation-enhanced Lewis lung carcinoma cell invasiveness in vitro and in pulmonary metastasis from inadequately irradiated primary tumor in vivo.

Targeted knockdown of MMP3 and MMP9 reduce primary tumor development and subsequent metastasis of aggressive adenocarcinoma cells. Nuclear MMP9 localized in central area of primary tumors and in lung-metastatic tumor nodules.