Requirement of matrix metalloproteinase-9 for the transformation of human mammary epithelial cells by Stat3-C

Dechow, Tobias; Pedranzini, Laura; Leitch, Andrea; Leslie, Kenneth; Gerald, William L.; Linkov, Irina; Bromberg, Jacqueline

doi:10.1073/pnas.0404100101

Cited by 241 publications

(211 citation statements)

References 39 publications

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“…In agreement with our study, S100A8 and S100A9 were shown to induce myeloid cell recruitment and tumor cell invasion in premetastatic lung (19). Interestingly, expression profiling of signal transducers and activators of transcription 3 -transformed MCF10A and HME breast epithelial cells identified 23 overexpressed genes including MMP-9, S100A8, and S100A9 (32). Taken together, S100A8 and S100A9 may serve as potential markers associated with tumor cell invasion and migration.…”

Section: Discussionsupporting

confidence: 74%

Global Gene Expression Profiling Unveils S100A8/A9 as Candidate Markers in H-Ras-Mediated Human Breast Epithelial Cell Invasion

Moon

Hao

Song

et al. 2008

Molecular Cancer Research

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The goal of the present study is to unveil the gene expression profile specific to the biological processes of human breast epithelial cell invasion and migration using an MCF10A model genetically engineered to constitutively activate the H-ras or N-ras signaling pathway. We previously showed that H-Ras, but not N-Ras, induces MCF10A cell invasion/migration, whereas both H-Ras and N-Ras induce cell proliferation and phenotypic transformation. Thus, these cell lines provide an experimental system to separate the gene expression profile associated with cell invasion apart from cell proliferation/transformation. Analysis of whole human genome microarray revealed that 412 genes were differentially expressed among MCF10A, N-Ras MCF10A, and H-Ras MCF10A cells and hierarchical clustering separated 412 genes into four clusters. We then tested whether S100A8 and S100A9, two of the genes which are most highly up-regulated in an H-Ras -specific manner, play a causative role for H-Ras -mediated MCF10A cell invasion and migration. Importantly, small interfering RNA -mediated knockdown of S100A8/A9 expression significantly reduced H-Ras -induced invasion/ migration. Conversely, the induction of S100A8/A9 expression conferred the invasive/migratory phenotype to parental MCF10A cells. Furthermore, we provided evidence of signaling cross-talk between S100A8/A9 and the mitogen-activated protein kinase signaling pathways essential for H-Ras -mediated cell invasion and migration. Taken together, this study revealed S100A8/A9 genes as candidate markers for metastatic potential of breast epithelial cells. Our gene profile data provide useful information which may lead to the identification of additional potential targets for the prognosis and/or therapy of metastatic breast cancer. (Mol Cancer Res 2008;6(10):1544 -53)

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Section: Discussionsupporting

confidence: 74%

Global Gene Expression Profiling Unveils S100A8/A9 as Candidate Markers in H-Ras-Mediated Human Breast Epithelial Cell Invasion

Moon

Hao

Song

et al. 2008

Molecular Cancer Research

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“…40 BcL-xL is one of the important regulators of apoptosis and is involved in the regulation of the cell cycle, prolongs cell survival and inhibits apoptosis. Stat3 normally resides in the cytoplasm and can be activated through phosphorylation by cytokines, growth factors and oncogenic proteins.…”

Section: Discussionmentioning

confidence: 99%

“…RNAi caused by synthetic siRNAs is transient due to lack of tumor-targeting and degradation of siRNA. 40 However, this problem has been solved here by using plasmid expression vectors in Salmonella as a delivery tool. These plasmid vectors produce sufficient amounts of shRNA using normal cellular machinery, 41 and are able to knockdown expression of target genes for extended periods of time.…”

Section: Discussionmentioning

confidence: 99%

Plasmid-based Survivin shRNA and GRIM-19 carried by attenuated Salmonella suppresses tumor cell growth

Liu

Zhang²,

Guo³

et al. 2012

Asian J Androl

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Persistent activation of Survivin and its overexpression contribute to the formation, progression and metastasis of several different tumor types. Therefore, Survivin is an ideal target for RNA interference mediated-growth inhibition. Blockade of Survivin using specific short hairpin RNAs (shRNA) can significantly reduce prostate tumor growth. RNA interference does not fully ablate target gene expression, owing to the idiosyncrasies associated with shRNAs and their targets. To enhance the therapeutic efficacy of Survivin-specific shRNA, we employed a combinatorial expression of Survivin-specific shRNA and gene associated with retinoid-interferon-induced mortality-19 (GRIM-19). Then, the GRIM-19 coding sequences and Survivin-specific shRNAs were used to create a dual expression plasmid vector and were carried by an attenuated strain of Salmonella enteric serovar typhimurium (S. typhimurium) to treat prostate cancer in vitro and in vivo. We found that the co-expressed Survivin-specific shRNA and GRIM-19 synergistically and more effectively inhibited prostate tumor proliferation and survival, when compared with treatment with either single agent alone in vitro and in vivo. This study has provided a novel cancer gene therapeutic approach for prostate cancer.

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“…34,35 STAT3 regulation of matrix metalloproteinase-2 (mmp-2) correlates with invasiveness of melanoma cells, 38 and activation of mmp-9 is required for STAT3-induced transformation of mammary epithelial cells. 50 Thus STAT3 and STAT5 contribute to cancer by activating genes that promote cell cycle entry and cell survival, among other cellular processes (Fig. 1).…”

Section: Stat Signaling and Cancermentioning

confidence: 99%

“…To directly evaluate the contribution of STAT3 to transformation of mammary epithelial cells, STAT3-C was expressed in these cells. 50 In two independent immortalized mammary epithelial cell lines, MCF10A and HMECs, STAT3-C expression led to transformation. To identify the changes in gene expression associated with this transformation, the expression profile of cells expressing STAT3-C was compared to cells expressing empty vector using Affymetrix oligonucleotide microarrays.…”

Section: Genome-wide Analysis Of Stat Targetsmentioning

confidence: 99%

Genome-wide analysis of STAT target genes: Elucidating the mechanism of STAT-mediated oncogenesis

Alvarez

Frank²

2004

Cancer Biology & Therapy

104

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Requirement of matrix metalloproteinase-9 for the transformation of human mammary epithelial cells by Stat3-C

Cited by 241 publications

References 39 publications

Global Gene Expression Profiling Unveils S100A8/A9 as Candidate Markers in H-Ras-Mediated Human Breast Epithelial Cell Invasion

Global Gene Expression Profiling Unveils S100A8/A9 as Candidate Markers in H-Ras-Mediated Human Breast Epithelial Cell Invasion

Plasmid-based Survivin shRNA and GRIM-19 carried by attenuated Salmonella suppresses tumor cell growth

Genome-wide analysis of STAT target genes: Elucidating the mechanism of STAT-mediated oncogenesis

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