ArticleCancer science2017
Insulin-like growth factor-1 signaling is responsible for cathepsin G-induced aggregation of breast cancer MCF-7 cells.
Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Aging changes the mechanism that underlies JAK2 modulation of neutrophil function.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Advances in Targeting Neutrophil Extracellular Traps as a Promising Approach for Breast Cancer Treatment.Combinatorial chemistry & high throughput screening · 2026Review
- Target neutrophil heterogeneity and plasticity in cancer.Journal of hematology & oncology · 2025Review
- Neutrophils in cancer: At the crucial crossroads of anti-tumor and pro-tumor.Cancer communications (London, England) · 2025Review
- Fenugreek inhibits cathepsin G activity and suppresses the progression of malignant phenotypes in MCF-7 cells.Biochemistry and biophysics reports · 2025Article
- Myeloid cells are involved in tumor immunity, metastasis and metabolism in tumor microenvironment.Cell biology and toxicology · 2025Review
- Metabolic reprogramming of tumor-associated neutrophils in tumor treatment and therapeutic resistance.Frontiers in cell and developmental biology · 2025Review
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- Identification of a biomarker to predict doxorubicin/cisplatin chemotherapy efficacy in osteosarcoma patients using primary, recurrent and metastatic specimens.Translational oncology · 2024Article
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- Targeting NETosis: nature's alarm system in cancer progression.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- The causal relationship between cathepsins and digestive system tumors: a Mendelian randomization study.Frontiers in oncology · 2024Article
- Insights into the Tumor Microenvironment-Components, Functions and Therapeutics.International journal of molecular sciences · 2023Review
- Inflammation in Prostate Cancer: Exploring the Promising Role of Phenolic Compounds as an Innovative Therapeutic Approach.Biomedicines · 2023Review
- Lactoferrin and Activated Protein C: Potential Role in Prevention of Cancer Progression and Recurrence.International journal of molecular and cellular medicine · 2023Review
- Prognostic value of systemic immune inflammation index and geriatric nutrition risk index in early-onset colorectal cancer.Frontiers in nutrition · 2023Article
- Mechanisms of esophageal cancer metastasis and treatment progress.Frontiers in immunology · 2023Review
- Heterogeneity of neutrophils in cancer: one size does not fit all.Cancer biology & medicine · 2022Review
- Article
- The feasibility of proteomics sequencing based immune-related prognostic signature for predicting clinical outcomes of bladder cancer patients.BMC cancer · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cathepsin G (CG), a neutrophil serine protease, induces cell migration and multicellular aggregation of human breast cancer MCF-7 cells in a process that is dependent on E-cadherin and CG enzymatic activity. While these tumor cell aggregates can cause tumor emboli that could represent intravascular growth and extravasation into the surrounding tissues, resulting in metastasis, the molecular mechanism underlying this process remains poorly characterized. In this study, we aimed to identify the signaling pathway that is triggered during CG-mediated stimulation of cell aggregation. Screening of a library of compounds containing approximately 90 molecular-targeting drugs revealed that this process was suppressed by the insulin-like growth factor-1 (IGF-1) receptor (IGF-1R)-specific kinase inhibitor OSI-906, as well as the multikinase inhibitors axitinib and sunitinib. Antibody array analysis, which is capable of detecting tyrosine phosphorylation of 49 distinct receptor tyrosine kinases, and the results of immunoprecipitation studies indicated that IGF-1R is phosphorylated in response to CG treatment. Notably, IGF-1R neutralization via treatment with a specific antibody or silencing of IGF-1R expression through siRNA transfection suppressed cell aggregation. Furthermore, CG treatment of MCF-7 cells resulted in increased release of IGF-1 into the medium for 24 h, while antibody-mediated IGF-1 neutralization partially prevented CG-induced cell aggregation. These results demonstrate that autocrine IGF-1 signaling is partly responsible for the cell aggregation induced by CG.
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