دورية أكاديمية
أعرض في EDS

Elucidating the role of the kinase activity of endothelial cell focal adhesion kinase in angiocrine signalling and tumour growth.

التفاصيل البيبلوغرافية
العنوان: Elucidating the role of the kinase activity of endothelial cell focal adhesion kinase in angiocrine signalling and tumour growth.
المؤلفون: Newport E; Centre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK., Pedrosa AR; Centre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK., Lees D; Centre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK., Dukinfield M; Centre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK., Carter E; Centre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK., Gomez-Escudero J; Centre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK., Casado P; Centre for Genomics and Computational Biology, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK., Rajeeve V; Centre for Genomics and Computational Biology, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK., Reynolds LE; Centre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK., R Cutillas P; Centre for Genomics and Computational Biology, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK., Duffy SW; Wolfson Institute, London, UK., De Luxán Delgado B; Centre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK., Hodivala-Dilke K; Centre for Tumour Microenvironment, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, London, UK.
المصدر: The Journal of pathology [J Pathol] 2022 Feb; Vol. 256 (2), pp. 235-247. Date of Electronic Publication: 2021 Dec 20.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: John Wiley And Sons Country of Publication: England NLM ID: 0204634 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1096-9896 (Electronic) Linking ISSN: 00223417 NLM ISO Abbreviation: J Pathol Subsets: MEDLINE
أسماء مطبوعة: Publication: Chichester : John Wiley And Sons
Original Publication: London, Oliver & Boyd.
مواضيع طبية MeSH: Neovascularization, Physiologic*, Endothelial Cells/*enzymology , Focal Adhesion Kinase 1/*metabolism , Melanoma, Experimental/*enzymology , Skin Neoplasms/*enzymology, Angiogenesis Inhibitors/pharmacology ; Animals ; Antibiotics, Antineoplastic/pharmacology ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Cytokines/metabolism ; Doxorubicin/pharmacology ; Drug Resistance, Neoplasm ; Female ; Focal Adhesion Kinase 1/antagonists & inhibitors ; Focal Adhesion Kinase 1/genetics ; Humans ; Male ; Melanoma, Experimental/drug therapy ; Melanoma, Experimental/genetics ; Melanoma, Experimental/pathology ; Mice, Inbred C57BL ; Mice, Knockout ; Protein Kinase Inhibitors/pharmacology ; Signal Transduction ; Skin Neoplasms/drug therapy ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology ; Tumor Burden ; Mice
مستخلص: A common limitation of cancer treatments is chemotherapy resistance. We have previously identified that endothelial cell (EC)-specific deletion of focal adhesion kinase (FAK) sensitises tumour cells to DNA-damaging therapies, reducing tumour growth in mice. The present study addressed the kinase activity dependency of EC FAK sensitisation to the DNA-damaging chemotherapeutic drug, doxorubicin. FAK is recognised as a therapeutic target in tumour cells, leading to the development of a range of inhibitors, the majority being ATP competitive kinase inhibitors. We demonstrate that inactivation of EC FAK kinase domain (kinase dead; EC FAK-KD) in established subcutaneous B16F0 tumours improves melanoma cell sensitisation to doxorubicin. Doxorubicin treatment in EC FAK-KD mice reduced the percentage change in exponential B16F0 tumour growth further than in wild-type mice. There was no difference in tumour blood vessel numbers, vessel perfusion or doxorubicin delivery between genotypes, suggesting a possible angiocrine effect on the regulation of tumour growth. Doxorubicin reduced perivascular malignant cell proliferation, while enhancing perivascular tumour cell apoptosis and DNA damage in tumours grown in EC FAK-KD mice 48 h after doxorubicin injection. Human pulmonary microvascular ECs treated with the pharmacological FAK kinase inhibitors defactinib, PF-562,271 or PF-573,228 in combination with doxorubicin also reduced cytokine expression levels. Together, these data suggest that targeting EC FAK kinase activity may alter angiocrine signals that correlate with improved acute tumour cell chemosensitisation. © 2021 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland.
(© 2021 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland.)
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معلومات مُعتمدة: 12007 United Kingdom CRUK_ Cancer Research UK; PG/18/75/34096 United Kingdom BHF_ British Heart Foundation; 18673 United Kingdom CRUK_ Cancer Research UK; MR/V009621/1 United Kingdom MRC_ Medical Research Council; 28990 United Kingdom CRUK_ Cancer Research UK
فهرسة مساهمة: Keywords: DNA-damaging therapy; FAK inhibitor; angiocrine signalling; cytokines; doxorubicin; endothelial cells; focal adhesion kinase activity
المشرفين على المادة: 0 (Angiogenesis Inhibitors)
0 (Antibiotics, Antineoplastic)
0 (Cytokines)
0 (Protein Kinase Inhibitors)
80168379AG (Doxorubicin)
EC 2.7.10.2 (Focal Adhesion Kinase 1)
EC 2.7.10.2 (PTK2 protein, human)
EC 2.7.10.2 (Ptk2 protein, mouse)
تواريخ الأحداث: Date Created: 20211107 Date Completed: 20220221 Latest Revision: 20240724
رمز التحديث: 20240725
DOI: 10.1002/path.5833
PMID: 34743335
قاعدة البيانات: MEDLINE
الوصف
تدمد:1096-9896
DOI:10.1002/path.5833