Down-regulation of TIMP-2 is associated with nonsmall cell lung carcinoma

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.

TFPI-2 downregulation can contribute to tumour invasion of lung cancer cells

Data indicate that TIMP-2 promotes an anti-tumoral transcriptional profile in lung cancer including upregulation of E-cadherin.

our results demonstrate that TIMP-2 stimulates lung adenocarcinoma cell proliferation

Tissue inhibitor of metallopeptidases 2 (TIMP2) protein and mRNA levels were downregulated after miR-15b overexpression in A549 and LTEP-a-2 cells, respectively. Our results indicate that high expression of miR-15b is associated with non-small cell lung cancer (NSCLC)and suggest that miR-15b expression may be a novel biomarker for predicting clinical outcomes in NSCLC patients

Released TIMP-2 is structurally intact and maintains the ability to inhibit MMP activity, as well as suppress lung cancer cell proliferation in vitro. These findings suggest that the AcVES3 hydrogel will be useful as an injectable vehicle for systemic delivery of TIMP-2 in vivo for ongoing preclinical development.

Low TIMP2 expression is associated with decrease in radiosensitivity of lung cancer.

MicroRNA-130b functions as an oncomiRNA in non-small cell lung cancer by targeting tissue inhibitor of metalloproteinase-2.

long noncoding RNA FENDRR suppressed the progression of non-small cell lung cancer via binding to miR-761 and regulating TIMP2 expression.

Spread of Lewis lung carcinoma cells from serum to lungs was associated with increased serum content of TIMP-1 and TIMP-2.