ArticleMediators of inflammation2014
Neutrophil cathepsin G, but not elastase, induces aggregation of MCF-7 mammary carcinoma cells by a protease activity-dependent cell-oriented mechanism.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Advances in Targeting Neutrophil Extracellular Traps as a Promising Approach for Breast Cancer Treatment.Combinatorial chemistry & high throughput screening · 2026Review
- Therapeutic potential of tumor-associated neutrophils: dual role and phenotypic plasticity.Signal transduction and targeted therapy · 2025Review
- Fenugreek inhibits cathepsin G activity and suppresses the progression of malignant phenotypes in MCF-7 cells.Biochemistry and biophysics reports · 2025Article
- Stroma-tology: Predicting recurrence in cholangiocarcinoma: Editorial on "Development and validation of a stromal-immune signature to predict prognosis in intrahepatic cholangiocarcinoma".Clinical and molecular hepatology · 2025Article
- MDSC: a new potential breakthrough in CAR-T therapy for solid tumors.Cell communication and signaling : CCS · 2024Review
- Insights into the Tumor Microenvironment-Components, Functions and Therapeutics.International journal of molecular sciences · 2023Review
- Exploiting innate immunity for cancer immunotherapy.Molecular cancer · 2023Review
- Extracellular matrix remodeling in the tumor immunity.Frontiers in immunology · 2023Review
- The Role of Neutrophils in the Pathogenesis of Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2021Review
- Review
- The Tumor Proteolytic Landscape: A Challenging Frontier in Cancer Diagnosis and Therapy.International journal of molecular sciences · 2021Review
- Interplay between Extracellular Matrix and Neutrophils in Diseases.Journal of immunology research · 2021Review
- Lysosomal peptidases in innate immune cells: implications for cancer immunity.Cancer immunology, immunotherapy : CII · 2020Review
- Neutrophils in the Tumor Microenvironment.Advances in experimental medicine and biology · 2020Review
- Tumor-Associated Neutrophils in Cancer: Going Pro.Cancers · 2019Review
- The dynamic change of neutrophil to lymphocyte ratio can predict clinical outcome in stage I-III colon cancer.Scientific reports · 2018Article
- Neutrophil count and percentage: potential independent prognostic indicators for advanced cancer patients in a palliative care setting.Oncotarget · 2017Article
- Insulin-like growth factor-1 signaling is responsible for cathepsin G-induced aggregation of breast cancer MCF-7 cells.Cancer science · 2017Article
- Neutrophils in Cancer: Two Sides of the Same Coin.Journal of immunology research · 2015Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously found that a neutrophil serine protease, cathepsin G, weakens adherence to culture substrates and induces E-cadherin-dependent aggregation of MCF-7 human breast cancer cells through its protease activity. In this study, we examined whether aggregation is caused by degradation of adhesion molecules on the culture substrates or through an unidentified mechanism. We compared the effect of treatment with cathepsin G and other proteases, including neutrophil elastase against fibronectin- (FN-) coated substrates. Cathepsin G and elastase potently degraded FN on the substrates and induced aggregation of MCF-7 cells that had been subsequently seeded onto the substrate. However, substrate-bound cathepsin G and elastase may have caused cell aggregation. After inhibiting the proteases on the culture substrates using the irreversible inhibitor phenylmethylsulfonyl fluoride (PMSF), we examined whether aggregation of MCF-7 cells was suppressed. PMSF attenuated cell aggregation on cathepsin G-treated substrates, but the effect was weak in cells pretreated with high concentrations of cathepsin G. In contrast, PMSF did not suppress cell aggregation on elastase-treated FN. Moreover, cathepsin G, but not elastase, induced aggregation on poly-L-lysine substrates which are not decomposed by these enzymes, and the action of cathepsin G was nearly completely attenuated by PMSF. These results suggest that cathepsin G induces MCF-7 aggregation through a cell-oriented mechanism.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.