Modulation of Breast Cancer Cell Function by Intracellular Signaling Through the Membrane-Type I Matrix Metalloproteinase

2000 ◽  
Author(s):  
Paolo Mignatti
Keyword(s):  
Breast Cancer ◽  
Matrix Metalloproteinase ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Intracellular Signaling ◽  
Cell Function ◽  
Type I ◽  
Membrane Type

scholarly journals Matrix Metalloproteinase 8 (Collagenase 2) Induces the Expression of Interleukins 6 and 8 in Breast Cancer Cells

2013 ◽  
Vol 288 (23) ◽  
pp. 16282-16294 ◽  
Author(s):  
Sally Thirkettle ◽  
Julie Decock ◽  
Hugh Arnold ◽  
Caroline J. Pennington ◽  
Diane M. Jaworski ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Matrix Metalloproteinase ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines

Matrix metalloproteinase 8 (MMP-8) is a tumor-suppressive protease that cleaves numerous substrates, including matrix proteins and chemokines. In particular, MMP-8 proteolytically activates IL-8 and, thereby, regulates neutrophil chemotaxis in vivo. We explored the effects of expression of either a WT or catalytically inactive (E198A) mutant version of MMP-8 in human breast cancer cell lines. Analysis of serum-free conditioned media from three breast cancer cell lines (MCF-7, SK-BR-3, and MDA-MB-231) expressing WT MMP-8 revealed elevated levels of IL-6 and IL-8. This increase was mirrored at the mRNA level and was dependent on MMP-8 catalytic activity. However, sustained expression of WT MMP-8 by breast cancer cells was non-permissive for long-term growth, as shown by reduced colony formation compared with cells expressing either control vector or E198A mutant MMP-8. In long-term culture of transfected MDA-MB-231 cells, expression of WT but not E198A mutant MMP-8 was lost, with IL-6 and IL-8 levels returning to base line. Rare clonal isolates of MDA-MB-231 cells expressing WT MMP-8 were generated, and these showed constitutively high levels of IL-6 and IL-8, although production of the interleukins was no longer dependent upon MMP-8 activity. These studies support a causal connection between MMP-8 activity and the IL-6/IL-8 network, with an acute response to MMP-8 involving induction of the proinflammatory mediators, which may in part serve to compensate for the deleterious effects of MMP-8 on breast cancer cell growth. This axis may be relevant to the recognized ability of MMP-8 to orchestrate the innate immune system in inflammation in vivo.

scholarly journals Role of secreted type I collagen derived from stromal cells in two breast cancer cell lines

2014 ◽  
Vol 8 (2) ◽  
pp. 507-512 ◽  
Author(s):  
SUNG HOON KIM ◽  
HYE YOON LEE ◽  
SEUNG PIL JUNG ◽  
SANGMIN KIM ◽  
JEONG EON LEE ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Stromal Cells ◽  
Type I Collagen ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Type I

The effect of tomatine on metastasis related matrix metalloproteinase (MMP) activities in breast cancer cell model

Gene ◽  
2017 ◽  
Vol 627 ◽  
pp. 408-411 ◽  
Author(s):  
Besra Özmen Yelken ◽  
Tuğçe Balcı ◽  
Sunde Yılmaz Süslüer ◽  
Çağla Kayabaşı ◽  
Çığır Biray Avcı ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Matrix Metalloproteinase ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Model ◽  
Breast Cancer Cell Model

scholarly journals PRMT1 regulates EGFR and Wnt signaling pathways and is a promising target for combinatorial treatment of breast cancer

2021 ◽  
Author(s):  
Samyuktha Suresh ◽  
Solène Huard ◽  
Amélie Brisson ◽  
Fariba Némati ◽  
Coralie Poulard ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Wnt Signaling ◽  
Signaling Pathways ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Xenograft Model ◽  
Growth Factor Receptor ◽  
Breast Cancer Cell Lines ◽  
Type I ◽  
Cancer Subtypes

Identifying new therapeutic strategies for triple-negative breast cancer (TNBC) patients is a priority as these patients are highly prone to relapse after chemotherapy. Here, we found that protein arginine methyltransferase 1 (PRMT1) is highly expressed in all breast cancer subtypes. Its depletion decreases cell survival by inducing DNA damage and apoptosis in various breast cancer cell lines. Transcriptomic analysis and chromatin immunoprecipitation revealed that PRMT1 regulates the epidermal growth factor receptor (EGFR) and the Wnt signaling pathways, reported to be activated in TNBC. The enzymatic activity of PRMT1 is also required to stimulate the canonical Wnt pathway. Recently developed type I PRMT inhibitors decrease breast cancer cell proliferation and show anti-tumor activity in a TNBC xenograft model. These inhibitors display synergistic interactions with some chemotherapies used to treat TNBC patients, as well as the EGFR inhibitor, erlotinib. Therefore, targeting PRMT1 in combination with drugs used in the clinic may improve current treatments for TNBC patients.

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