ArticleBMC cancer2007
Stromelysin-3 over-expression enhances tumourigenesis in MCF-7 and MDA-MB-231 breast cancer cell lines: involvement of the IGF-1 signalling pathway.
Article in BMC cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 48 citations in OpenAlex.
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- Matrix Metalloproteinase 11 Promotes Migration and Invasion of Colorectal Cancer by Elevating Slug Protein.International journal of medical sciences · 2024Article
- Identification and comprehensive analysis of epithelial-mesenchymal transition related target genes of miR-222-3p in breast cancer.Frontiers in oncology · 2023Article
- Multiple Cell Cultures for MRI Analysis.International journal of molecular sciences · 2022Review
- Matrix metalloproteinase 11 (MMP11) in macrophages promotes the migration of HER2-positive breast cancer cells and monocyte recruitment through CCL2-CCR2 signaling.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Matrix metalloproteinases as therapeutic targets in breast cancer.Frontiers in oncology · 2022Review
- High MMP-11 expression associated with low CD8+ T cells decreases the survival rate in patients with breast cancer.PloS one · 2021Article
- An integrated bioinformatics analysis of potential therapeutic targets among matrix metalloproteinases in breast cancer.Oncology letters · 2019Article
- MMP11 and CD2 as novel prognostic factors in hormone receptor-negative, HER2-positive breast cancer.Breast cancer research and treatment · 2017Article
- MicroRNA-145 functions as a tumor suppressor by targeting matrix metalloproteinase 11 and Rab GTPase family 27a in triple-negative breast cancer.Cancer gene therapy · 2016Article
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- Rad51 supports triple negative breast cancer metastasis.Oncotarget · 2014Article
- mRNA profiling of the cancer degradome in oesophago-gastric adenocarcinoma.British journal of cancer · 2012Article
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- Molecular and functional ultrasound imaging in differently aggressive breast cancer xenografts using two novel ultrasound contrast agents (BR55 and BR38).European radiology · 2011Article
- Gli1 enhances migration and invasion via up-regulation of MMP-11 and promotes metastasis in ERα negative breast cancer cell lines.Clinical & experimental metastasis · 2011Article
- CNK1 is a novel Akt interaction partner that promotes cell proliferation through the Akt-FoxO signalling axis.Oncogene · 2010Article
- Systemic in vivo distribution of activatable cell penetrating peptides is superior to that of cell penetrating peptides.Integrative biology : quantitative biosciences from nano to macro · 2009Article
- Epithelial to mesenchymal transition and breast cancer.Breast cancer research : BCR · 2009Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStromelysin-3 (ST-3) is over-expressed in the majority of human carcinomas including breast carcinoma. Due to its known effect in promoting tumour formation, but its impeding effect on metastasis, a dual role of ST-3 in tumour progression, depending on the cellular grade of dedifferentiation, was hypothesized.
methodsThe present study was designed to investigate the influence of ST-3 in vivo and in vitro on the oestrogen-dependent, non-invasive MCF-7 breast carcinoma cell line as well as on the oestrogen-independent, invasive MDA-MB-231 breast carcinoma cell line. Therefore an orthotopic human xenograft tumour model in nude mice, as well as a 3D matrigel cell culture system, were employed.
resultsUsing both in vitro and in vivo techniques, we have demonstrated that over-expression of ST-3 in MCF-7 and MDA-MB-231 cells leads to both increased cell numbers and tumour volumes. This observation was dependent upon the presence of growth factors. In particular, the enhanced proliferative capacity was in MCF-7/ST-3 completely and in MDA-MB-231/ST-3 cells partially dependent on the IGF-1 signalling pathway. Microarray analysis of ST-3 over-expressing cells revealed that in addition to cell proliferation, further biological processes seemed to be affected, such as cell motility and stress response. The MAPK-pathway as well as the Wnt and PI3-kinase pathways, appear to also play a potential role. Furthermore, we have demonstrated that breast cancer cell lines of different differentiation status, as well as the non-tumourigenic cell line MCF-10A, have a comparable capability to induce endogenous ST-3 expression in fibroblasts.
conclusionThese data reveal that ST-3 is capable of enhancing tumourigenesis in highly differentiated "early stage" breast cancer cell lines as well as in further progressed breast cancer cell lines that have already undergone epithelial-mesenchymal transition. We propose that ST-3 induction in tumour fibroblasts leads to the stimulation of the IGF-1R pathway in carcinoma cells, thus enhancing their proliferative capacity. In addition, further different cellular processes seem to be activated by ST-3, possibly accounting for the dual role of ST-3 in tumour progression and metastasis.
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