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Expression data from HeLa cells with and without human recombinant TIMP-4 treatment

ABSTRACT: TIMP-4 overexpression increases tumor burden in mice, promotes progenitor cell phenotype and sensitizes cells to apoptosis, by relying on NFkB signaling

ORGANISM(S): Homo sapiens

PROVIDER: GSE60671 | GEO | 2015/11/25

SECONDARY ACCESSION(S): PRJNA259221

REPOSITORIES: GEO

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Expression data from HeLa cells with and without human recombinant TIMP-4 treatment

Project description:TIMP-4 overexpression increases tumor burden in mice, promotes progenitor cell phenotype and sensitizes cells to apoptosis, by relying on NFkB signaling We used microarrays to detail the molecules and signal transduction pathways modulated by hrTIMP-4

2015-11-25 | E-GEOD-60671 | biostudies-arrayexpress

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

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

Project description: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.

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Gemcitabine induced TIMP-1 attenuates therapy response and promotes tumour growth and liver metastasis in pancreatic cancer

Project description:Gemcitabine constitutes one of the backbones for chemotherapy treatment in pancreatic ductal adenocarcinoma (PDAC) but patients often show poor or complete lack of response to this agent. Molecular markers downstream of Gemcitabine treatment in pre-clinical models may provide an insight into resistance mechanisms. We identified potential secretory biomarkers of Gemcitabine resistance (response) in the transgenic KRasG12D; Trp53R172H; Pdx-1 Cre (KPC) mouse model of PDAC using cytokine arrays. We validated the oncogenic role of the cytokine tissue inhibitor of matrix metalloproteinases 1 (TIMP-1) in primary pancreatic tumours and metastasis using both in vitro techniques and animal models. We identified potential pathways affected downstream of TIMP-1 using the Illumina Human H12 array. Our findings were validated in both primary and metastatic models of pancreatic cancer. Gemcitabine increases inflammatory cytokines including TIMP-1 in the KPC mouse model. TIMP-1 is upregulated in patients with pancreatic intraepithelial neoplasias grade 3 and PDAC lesions relative to matched normal pancreatic tissue. Additionally, we demonstrate that TIMP-1 plays a role in tumour proliferation and angiogenesis, while inhibition resensitises to gemcitabine and radiotherapy. Strikingly, serum TIMP-1 levels support the formation of liver metastasis through the recruitment of immunosuppressive cell populations, such as CD11b+Gr1+ myeloid cells and CD4+CD25+FOXP3+ Tregs to the hepatic microenvironment. Gemcitabine treatment results in upregulation of the pro-tumourigenic/pro-metastatic cytokine TIMP-1, which partially explains the therapeutic resistance and poor responses to this therapy in PDAC. Our study provides a rationale for the development and testing of TIMP-1 specific inhibitors in addition to chemo/radiotherapy.

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TIMP-GLIA (gliadin nanoparticle) treatment in transgenic mice expressing celiac disease associated HLA-DQ8

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Loss of Timp gene family is sufficient for the acquisition of the CAF-like cell state

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TIMP-GLIA (gliadin nanoparticle) treatment in transgenic mice expressing celiac disease associated HLA-DQ8

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