MMP-7 is involved in the aging of primary human mammary epithelial cells (HMEC)

Bertram, Catharina; Hass, Ralf

doi:10.1016/j.exger.2007.11.007

Cited by 27 publications

(35 citation statements)

References 27 publications

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“…1A). These growth-stimulatory effects by MSC predominantly required direct intercellular communication, as co-culture experiments performed in transwells carrying a sterile track-etched membrane with 0.4 mm sized-pores revealed no detectable effects in proliferative capacity similar to previous studies (data not shown) [25]. Direct cell counting of MCF-7 cherry cells in co-culture with MSC GFP was also performed and compared with an appropriate amount of mono-cultured cells and confirmed a growth induction of the breast cancer cell line in contrast to a reduced MSC GFP cell number during co-culture (Supplementary Fig.…”

Section: Facs Separation Rna Isolation and Microarray Analysis Of Csupporting

confidence: 65%

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Human Mesenchymal Stroma/Stem Cells Exchange Membrane Proteins and Alter Functionality During Interaction with Different Tumor Cell Lines

Yang

Otte

Hass

2015

Stem Cells and Development

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To analyze effects of cellular interaction between human mesenchymal stroma/stem cells (MSC) and different cancer cells, direct co-cultures were performed and revealed significant growth stimulation of the tumor populations and a variety of protein exchanges. More than 90% of MCF-7 and primary human HBCEC699 breast cancer cells as well as NIH:OVCAR-3 ovarian adenocarcinoma cells acquired CD90 proteins during MSC co-culture, respectively. Furthermore, SK-OV-3 ovarian cancer cells progressively elevated CD105 and CD90 proteins in co-culture with MSC. Primary small cell hypercalcemic ovarian carcinoma cells (SCCOHT-1) demonstrated undetectable levels of CD73 and CD105; however, both proteins were significantly increased in the presence of MSC. This co-culture-mediated protein induction was also observed at transcriptional levels and changed functionality of SCCOHT-1 cells by an acquired capability to metabolize 5¢cAMP. Moreover, exchange between tumor cells and MSC worked bidirectional, as undetectable expression of epithelial cell adhesion molecule (EpCAM) in MSC significantly increased after co-culture with SK-OV-3 or NIH:OVCAR-3 cells. In addition, a small population of chimeric/hybrid cells appeared in each MSC/tumor cell co-culture by spontaneous cell fusion. Immune fluorescence demonstrated nanotube structures and exosomes between MSC and tumor cells, whereas cytochalasin-D partially abolished the intercellular protein transfer. More detailed functional analysis of FACS-separated MSC and NIH:OVCAR-3 cells after co-culture revealed the acquisition of epithelial cell-specific properties by MSC, including increased gene expression for cytokeratins and epithelial-like differentiation factors. Vice versa, a variety of transcriptional regulatory genes were downmodulated in NIH:OVCAR-3 cells after co-culture with MSC. Together, these mutual cellular interactions contributed to functional alterations in MSC and tumor cells.

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Section: Facs Separation Rna Isolation and Microarray Analysis Of Csupporting

confidence: 65%

“…Primary cultures of normal human mammary epithelial cells (HMEC) were commercially provided by BioWhittaker, Inc. (Lot #1F1012). Juvenile and proliferating HMEC in P13 were cultured at 2,500 cells/cm 2 in mammary epithelial cell growth medium (PromoCell) as previously described [25].…”

Section: Cell Culturementioning

confidence: 99%

Human Mesenchymal Stroma/Stem Cells Exchange Membrane Proteins and Alter Functionality During Interaction with Different Tumor Cell Lines

Yang

Otte

Hass

2015

Stem Cells and Development

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“…This MMP-1 effect on pre-senescent cells is thus quite opposite to the previously reported proangiogenic activities on proliferative EC (6). Also, an increase of a senescent-like phenotype was noted in a medulloblastoma cell line after down-regulation of MMP-9 by siRNAs (20) as well as in human mammary epithelial cells after siRNA-dependent down-regulation of MMP-7 (19). In the absence of lithium treatment, there was a trend for an increase of the appearance of SA-␤-galactosidase-positive cells in BAEC after down-regulation of MMP-1 (1.2-fold), which did not reach statistical significance (Fig.…”

Section: Discussionmentioning

confidence: 51%

“…A possible involvement of MMPs in the establishment of cell senescence has also been recently studied. Down-regulation of MMP-7, which is another target gene of the Wnt/␤-catenin signaling pathway (18), has been shown to enhance senescence of primary human mammary epithelial cells (19). Similarly, the down-regulation of MMP-9 in medulloblastoma cells triggered a cell cycle arrest and a senescent-like phenotype both in vitro and in a tumorigenesis model in vivo (20).…”

Section: Endothelial Cell (Ec)mentioning

confidence: 99%

Enhanced Endothelial Cell Senescence by Lithium-induced Matrix Metalloproteinase-1 Expression

Struewing

Durham

Barnett

et al. 2009

Journal of Biological Chemistry

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Endothelial cell (EC) senescence and dysfunction occurring after chronic injury and inflammation are highly associated with the development and progression of cardiovascular diseases. However, the factors involved in the establishment of EC senescence remain poorly understood. We have previously shown that lithium, an inhibitor of glycogen synthase kinase (GSK)-3␤ and activator of the Wnt/␤-catenin signaling pathway, induces an EC senescent-like phenotype. Herein, we show that lithium induces a rapid and pronounced up-regulation of the matrix metalloproteinase (MMP)-1, an inflammation and senescent cell marker, at the mRNA and protein levels, whereas the induction of two other senescent cell markers is either weak (interleukin-8) or delayed (plasminogen activator inhibitor-1). Lithium effect on MMP-1 expression is also specific among other Endothelial cell (EC)2 senescence and dysfunctions are the hallmarks of cardiovascular degenerative diseases such as atherosclerosis (1, 2). Senescent EC are characterized by changes in cell morphology and metabolism as well as by an irreversible cell cycle arrest and reduced migratory behavior (2), which account for impaired wound healing and slower tumor growth in the elderly (3). The senescent EC, like other cell types, display also changes in their secretory pattern with in particular, an increase of proinflammatory and proangiogenic factors, which in turn alters the tissue microenvironment and activity of neighboring cells (2-4). Although the effects of these proinflammatory and angiogenic factors on enabled-proliferative EC have been extensively studied, less is known about their effects on cell cycle-arrested and pre-senescent EC.The human matrix metalloproteinase (MMP)-1 and the plasminogen-activator inhibitor (PAI)-1 belong to this class of proinflammatory and proangiogenic factors, which control vascular remodeling and angiogenesis by regulating extracellular matrix (ECM) degradation and release of growth factors such as transforming growth factor-␤ and vascular endothelial growth factor (5, 6). By inducing both angiogenesis and changes in the ECM microenvironment, MMP-1 up-regulation has been associated with increased tumor growth and metastasis (6, 7). PAI-1 has a dual effect on angiogenesis depending upon its level of expression and the status of the ECM proteolytic system (5). On the other hand, the expressions of MMP-1 and PAI-1 are increased in senescent EC in culture (8, 9) and in vivo within atherosclerotic lesions (10). MMP-1 activity is in particular associated with instability of the atherosclerotic plaque and subsequently with infarct events in humans (11). Increased PAI-1 levels are also associated with a poor prognostic in atherosclerosis and cardiovascular disease progression (12).Interestingly, PAI-1 up-regulation has been associated with the establishment of cell senescence both in vitro and in vivo (13). PAI-1 is a downstream target gene of the tumor suppressor p53 (14) and is required for p53-induced cell senescence in primary fibroblasts via its ...

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“…The resulting failure to activate Fra-1 via the missing ICD induces tropoelastin formation, subsequent cleavage by lysyl oxidases, and extracellular formation of elastin fibers. Consequently, signaling in senescent HMEC with altered MMP7 levels has been attributed to increased fibrosis as a prerequisite for breast cancer development [53–55]. …”

Section: Introductionmentioning

confidence: 99%

Breast Carcinoma: From Initial Tumor Cell Detachment to Settlement at Secondary Sites

Melzer

Ohe

Hass

2017

BioMed Research International

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Metastasis represents a multistep cascade of cancer cell alterations accompanied by structural and functional changes within the tumor microenvironment which may involve the induction of a retrodifferentiation program. Major steps in metastatic developments include (A) cell detachment from the primary tumor site involving epithelial-mesenchymal transition (EMT), (B) migration and invasion into surrounding tissue, (C) transendothelial intravasation into the vasculature of blood and/or lymphatic vessels as circulating tumor cells (CTCs), (D) dissemination to distant organs, and (E) extravasation of CTCs to secondary sites as disseminated tumor cells (DTCs). This article highlights some aspects of the metastatic cascade with a focus on breast cancer cells. Metastatic steps critically depend on the capability of cancer cells to adapt to distant tissues and the corresponding new microenvironment. As a consequence, increasing plasticity and developmental changes paralleled by acquisition of new cancer cell functionalities challenge a successful therapeutic approach.

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MMP-7 is involved in the aging of primary human mammary epithelial cells (HMEC)

Cited by 27 publications

References 27 publications

Human Mesenchymal Stroma/Stem Cells Exchange Membrane Proteins and Alter Functionality During Interaction with Different Tumor Cell Lines

Human Mesenchymal Stroma/Stem Cells Exchange Membrane Proteins and Alter Functionality During Interaction with Different Tumor Cell Lines

Enhanced Endothelial Cell Senescence by Lithium-induced Matrix Metalloproteinase-1 Expression

Breast Carcinoma: From Initial Tumor Cell Detachment to Settlement at Secondary Sites

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