دورية أكاديمية
أعرض في EDS

Eicosanoid regulation of debris-stimulated metastasis.

التفاصيل البيبلوغرافية
العنوان: Eicosanoid regulation of debris-stimulated metastasis.
المؤلفون: Deng J; Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Shaanxi Key Laboratory of Degradable Biomedical Materials, School of Chemical Engineering, Northwest University, Xi'an 710069, China., Yang H; Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China., Haak VM; Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215., Yang J; Department of Entomology and Nematology, University of California, Davis, CA 95616.; UCD Comprehensive Cancer Center, University of California, Davis, CA 95616., Kipper FC; Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215., Barksdale C; Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215., Hwang SH; Department of Entomology and Nematology, University of California, Davis, CA 95616.; UCD Comprehensive Cancer Center, University of California, Davis, CA 95616., Gartung A; Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215., Bielenberg DR; Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115., Subbian S; Public Health Research Institute, New Jersey Medical School, Rutgers University, Newark, NJ07103., Ho KK; Shenzhen Bay Laboratory, Gaoke Innovation Center, Shenzhen 518000, China., Ye X; Shenzhen Bay Laboratory, Gaoke Innovation Center, Shenzhen 518000, China.; Institute of Biopharmaceutical and Health Engineering, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, China., Fan D; Shaanxi Key Laboratory of Degradable Biomedical Materials, School of Chemical Engineering, Northwest University, Xi'an 710069, China., Sun Y; Shenzhen Bay Laboratory, Gaoke Innovation Center, Shenzhen 518000, China; yongkui.sun@ionovabio.com bdhammock@ucdavis.edu dpanigra@bidmc.harvard.edu.; Institute of Biopharmaceutical and Health Engineering, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, China.; Division of Discovery Research, Ionova Life Science Co., Ltd., Shenzhen 518118, China.; Division of Discovery Research, Ionova Biotherapeutics Co., Inc., Foshan 528000, China., Hammock BD; Department of Entomology and Nematology, University of California, Davis, CA 95616; yongkui.sun@ionovabio.com bdhammock@ucdavis.edu dpanigra@bidmc.harvard.edu.; UCD Comprehensive Cancer Center, University of California, Davis, CA 95616., Panigrahy D; Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215; yongkui.sun@ionovabio.com bdhammock@ucdavis.edu dpanigra@bidmc.harvard.edu.; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.; Cancer Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.
المصدر: Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2021 Oct 12; Vol. 118 (41).
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: National Academy of Sciences Country of Publication: United States NLM ID: 7505876 Publication Model: Print Cited Medium: Internet ISSN: 1091-6490 (Electronic) Linking ISSN: 00278424 NLM ISO Abbreviation: Proc Natl Acad Sci U S A Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Washington, DC : National Academy of Sciences
مواضيع طبية MeSH: Eicosanoids/*metabolism , Epoxide Hydrolases/*biosynthesis , Macrophages/*immunology , Neoplasm Metastasis/*pathology , Receptors, Prostaglandin E, EP4 Subtype/*biosynthesis, Animals ; Antineoplastic Agents/adverse effects ; Antineoplastic Agents/therapeutic use ; Carcinoma, Hepatocellular/pathology ; Cell Death/drug effects ; Cell Line, Tumor ; Cytokine Release Syndrome/immunology ; Cytokine Release Syndrome/prevention & control ; Cytokines/metabolism ; Hep G2 Cells ; Humans ; Liver Neoplasms/drug therapy ; Liver Neoplasms/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Neoplasm Metastasis/prevention & control ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/pathology ; Phagocytosis/immunology ; RAW 264.7 Cells
مستخلص: Cancer therapy reduces tumor burden via tumor cell death ("debris"), which can accelerate tumor progression via the failure of inflammation resolution. Thus, there is an urgent need to develop treatment modalities that stimulate the clearance or resolution of inflammation-associated debris. Here, we demonstrate that chemotherapy-generated debris stimulates metastasis by up-regulating soluble epoxide hydrolase (sEH) and the prostaglandin E 2 receptor 4 (EP4). Therapy-induced tumor cell debris triggers a storm of proinflammatory and proangiogenic eicosanoid-driven cytokines. Thus, targeting a single eicosanoid or cytokine is unlikely to prevent chemotherapy-induced metastasis. Pharmacological abrogation of both sEH and EP4 eicosanoid pathways prevents hepato-pancreatic tumor growth and liver metastasis by promoting macrophage phagocytosis of debris and counterregulating a protumorigenic eicosanoid and cytokine storm. Therefore, stimulating the clearance of tumor cell debris via combined sEH and EP4 inhibition is an approach to prevent debris-stimulated metastasis and tumor growth.
Competing Interests: Competing interest statement: Y.S., K.-K.H., X.Y., and B.D.H. work with Ionova and EicOsis, respectively, on the development of EP4 and epoxide hydrolase inhibitors for clinical use. D.P., A.G., and B.D.H., and colleagues C. N. Serhan and P. Sime were coauthors on an earlier commentary suggesting modulating the eicosanoid and cytokine storms with a soluble epoxide hydrolase inhibitor to modulate severity of COVID infections, introducing the same mechanism as is suggested here for reduction of the cytokine storm following cancer therapy.
(Copyright © 2021 the Author(s). Published by PNAS.)
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معلومات مُعتمدة: P42 ES004699 United States ES NIEHS NIH HHS; R35 ES030443 United States ES NIEHS NIH HHS
فهرسة مساهمة: Keywords: autacoid; debris; inflammation resolution; prostaglandin E2 receptor 4; soluble epoxide hydrolase
المشرفين على المادة: 0 (Antineoplastic Agents)
0 (Cytokines)
0 (Eicosanoids)
0 (Ptger4 protein, mouse)
0 (Receptors, Prostaglandin E, EP4 Subtype)
EC 3.3.2.- (Epoxide Hydrolases)
EC 3.3.2.10 (Ephx2 protein, mouse)
تواريخ الأحداث: Date Created: 20211005 Date Completed: 20211214 Latest Revision: 20211214
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC8521662
DOI: 10.1073/pnas.2107771118
PMID: 34607951
قاعدة البيانات: MEDLINE
الوصف
تدمد:1091-6490
DOI:10.1073/pnas.2107771118