Regulation of intercellular biomolecule transfer-driven tumor angiogenesis and responses to anticancer therapies.

Szczegóły
Abstrakt

Tytuł:: Regulation of intercellular biomolecule transfer-driven tumor angiogenesis and responses to anticancer therapies.
Autorzy:: Lu Z; Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Ortiz A; Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Verginadis II; Department of Radiation Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Peck AR; Department of Chemistry, School of Arts and Sciences, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Zahedi F; Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Cho C; Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Yu P; Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
DeRita RM; Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Zhang H; Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Kubanoff R; Department of Chemistry, School of Arts and Sciences, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Sun Y; Department of Pathology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Yaspan AT; Department of Pathology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Krespan E; Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Beiting DP; Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Radaelli E; Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Ryeom SW; Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Diehl JA; Department of Biochemistry, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA.
Rui H; Department of Pathology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Koumenis C; Department of Radiation Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Fuchs SY; Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Źródło:: The Journal of clinical investigation [J Clin Invest] 2021 May 17; Vol. 131 (10).
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural
Język:: English
Imprint Name(s):: Publication: 1999- : Ann Arbor, MI : American Society for Clinical Investigation
Original Publication: New Haven [etc.] American Society for Clinical Investigation.
MeSH Terms:: Neoplasm Proteins*/antagonists & inhibitors
Neoplasm Proteins*/genetics
Neoplasm Proteins*/metabolism
Steroid Hydroxylases*/antagonists & inhibitors
Steroid Hydroxylases*/genetics
Steroid Hydroxylases*/metabolism
Neoplasms, Experimental/*drug therapy
Neovascularization, Pathologic/*drug therapy
Reserpine/*pharmacology
Sunitinib/*pharmacology
Animals ; Endothelial Cells/enzymology ; Gene Knockdown Techniques ; HCT116 Cells ; Humans ; Mice ; Mice, Knockout ; Neoplasm Metastasis ; Neoplasms, Experimental/enzymology ; Neoplasms, Experimental/genetics ; Neovascularization, Pathologic/enzymology ; Neovascularization, Pathologic/genetics
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Grant Information:: P01 CA165997 United States CA NCI NIH HHS; R01 CA240814 United States CA NCI NIH HHS; R01 CA247803 United States CA NCI NIH HHS
Contributed Indexing:: Keywords: Colorectal cancer; Endothelial cells; Oncology; Vascular Biology
Substance Nomenclature:: 0 (Neoplasm Proteins)
8B1QWR724A (Reserpine)
EC 1.14.- (Steroid Hydroxylases)
EC 1.14.99.38 (cholesterol 25-hydroxylase)
V99T50803M (Sunitinib)
Entry Date(s):: Date Created: 20210517 Date Completed: 20211005 Latest Revision: 20240402
Update Code:: 20240402
PubMed Central ID:: PMC8121529
DOI:: 10.1172/JCI144225
PMID:: 33998600
: Czasopismo naukowe

Intercellular biomolecule transfer (ICBT) between malignant and benign cells is a major driver of tumor growth, resistance to anticancer therapies, and therapy-triggered metastatic disease. Here we characterized cholesterol 25-hydroxylase (CH25H) as a key genetic suppressor of ICBT between malignant and endothelial cells (ECs) and of ICBT-driven angiopoietin-2-dependent activation of ECs, stimulation of intratumoral angiogenesis, and tumor growth. Human CH25H was downregulated in the ECs from patients with colorectal cancer and the low levels of stromal CH25H were associated with a poor disease outcome. Knockout of endothelial CH25H stimulated angiogenesis and tumor growth in mice. Pharmacologic inhibition of ICBT by reserpine compensated for CH25H loss, elicited angiostatic effects (alone or combined with sunitinib), augmented the therapeutic effect of radio-/chemotherapy, and prevented metastatic disease induced by these regimens. We propose inhibiting ICBT to improve the overall efficacy of anticancer therapies and limit their prometastatic side effects.

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