Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional profiles of TIMP-2 and Ala+TIMP-2 A549 overexpressing cells and in tumor xenografts.

ABSTRACT: TIMP-2 is an endogenous angiogenesis inhibitor, i.e. inhibits endothelial cell proliferation and tumor angiogenesis. As a result, TIMP-2 inhibits tumor growth and progression to metastasis. Understanding, therefore, the mechanisms of TIMP-2-mediated tumor growth inhibition would provide further support on the use of TIMP-2 as a novel biological agent for cancer therapy. We used microarray analysis to determine the TIMP-2 and Ala+TIMP-2 transcriptional profiles of A549 cancer cells in order to understand how TIMP-2 inhibits tumor growth and angiogenesis. We overexpressed TIMP-2 and its mutant (does not inhibit MMP) in A549 human lung cancer cells and determined TIMP-2 and Ala+TIMP-2 transcriptional profiles, groups of genes and associated biological functions. We then injected the cells in NOD-SCID mice and RNA from tumors were isolated for further analysis to identify genes that are associated with tumor growth inhibition.

ORGANISM(S): Homo sapiens

SUBMITTER: DIMITRA BOURBOULIA 

PROVIDER: E-GEOD-38408 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

TIMP-2 modulates cancer cell transcriptional profile and enhances E-cadherin/beta-catenin complex expression in A549 lung cancer cells.

Bourboulia Dimitra D   Han HuiYing H   Jensen-Taubman Sandra S   Gavil Noah N   Isaac Biju B   Wei Beiyang B   Neckers Len L   Stetler-Stevenson William G WG  

Oncotarget 20130101 1

Tissue Inhibitor of Metalloproteinase 2 (TIMP-2) plays an essential role in regulating matrix remodeling, cell growth, differentiation, angiogenesis and apoptosis in vitro and in vivo. We have recently shown that TIMP-2-mediated inhibition of tumor growth is independent of matrix metalloproteinase-mediated mechanisms, and is a consequence of modulating both the tumor cells and the tumor microenvironment. In the current study we aim to identify the molecular pathways associated with these effects  ...[more]

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