ArticleThe Journal of biological chemistry2019
Overexpression of the C-domain of angiotensin-converting enzyme reduces melanoma growth by stimulating M1 macrophage polarization.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Bioengineered iPSC-derived human macrophages with increased angiotensin-converting enzyme (ACE) expression suppress solid tumor growth.Signal transduction and targeted therapy · 2026Article
- Advanced nanotherapies for precision treatment of inflammatory lung diseases.Bioactive materials · 2025Review
- DDX54 downregulation enhances anti-PD1 therapy in immune-desert lung tumors with high tumor mutational burden.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Peroxisome proliferator-activated receptor alpha is an essential factor in enhanced macrophage immune function induced by angiotensin-converting enzyme.Cellular & molecular immunology · 2025Article
- Editorial: Hiding features in myeloid cells: metabolism preference in different disease models.Frontiers in immunology · 2025Article
- Fecal Carriage of Multidrug-ResistantBioMed research international · 2025Article
- Proteomic Analysis of Human Macrophages Overexpressing Angiotensin-Converting Enzyme.International journal of molecular sciences · 2024Article
- ACE Loss Drives Renal Cell Carcinoma Growth and Invasion by Modulating AKT-FOXO1.Biologics : targets & therapy · 2024Article
- Pocket ACEs: Discovering new function within an old player.Frontiers in physiology · 2023Review
- Editorial: Role of angiotensin-converting enzyme in myeloid immune functions.Frontiers in physiology · 2023Article
- The non-cardiovascular actions of ACE.Peptides · 2022Article
- Nanoporous titanium implant surface promotes osteogenesis by suppressing osteoclastogenesis via integrin β1/FAKpY397/MAPK pathway.Bioactive materials · 2022Article
- Exploring the Impact of ACE Inhibition in Immunity and Disease.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2022Review
- Protective effects of blocking PD-1 pathway on retinal ganglion cells in a mouse model of chronic ocular hypertension.Frontiers in immunology · 2022Article
- An ACE inhibitor reduces bactericidal activity of human neutrophils in vitro and impairs mouse neutrophil activity in vivo.Science translational medicine · 2021Article
- Astragaloside IV Alleviates the Experimental DSS-Induced Colitis by Remodeling Macrophage Polarization Through STAT Signaling.Frontiers in immunology · 2021Article
- Inhibitory Effect of Dihydroartemisinin on the Proliferation and Migration of Melanoma Cells and Experimental Lung Metastasis From Melanoma in Mice.Frontiers in pharmacology · 2021Article
- A Nomogram Combining a Four-Gene Biomarker and Clinical Factors for Predicting Survival of Melanoma.Frontiers in oncology · 2021Article
- Angiotensin-converting enzyme (ACE) inhibitor prescription affects non-small-cell lung cancer (NSCLC) patients response to PD-1/PD-L1 immune checkpoint blockers.Oncoimmunology · 2020Article
- LncGBP9/miR-34a axis drives macrophages toward a phenotype conducive for spinal cord injury repair via STAT1/STAT6 and SOCS3.Journal of neuroinflammation · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Angiotensin-converting enzyme (ACE) can hydrolyze many peptides and plays a central role in controlling blood pressure. Moreover, ACE overexpression in monocytes and macrophages increases resistance of mice to tumor growth. ACE is composed of two independent catalytic domains. Here, to investigate the specific role of each domain in tumor resistance, we overexpressed either WT ACE (Tg-ACE mice) or ACE lacking N- or C-domain catalytic activity (Tg-NKO and Tg-CKO mice) in the myeloid cells of mice. Tg-ACE and Tg-NKO mice exhibited strongly suppressed growth of B16-F10 melanoma because of increased ACE expression in macrophages, whereas Tg-CKO mice resisted melanoma no better than WT animals. The effect of ACE overexpression reverted to that of the WT enzyme with an ACE inhibitor but not with an angiotensin II type 1 (AT1) receptor antagonist. ACE C-domain overexpression in macrophages drove them toward a pronounced M1 phenotype upon tumor stimulation, with increased activation of NF-κB and signal transducer and activator of transcription 1 (STAT1) and decreased STAT3 and STAT6 activation. Tumor necrosis factor α (TNFα) is important for M1 activation, and TNFα blockade reverted Tg-NKO macrophages to a WT phenotype. Increased ACE C-domain expression increased the levels of reactive oxygen species (ROS) and of the transcription factor C/EBPβ in macrophages, important stimuli for TNFα expression, and decreased expression of several M2 markers, including interleukin-4Rα. Natural ACE C-domain-specific substrates are not well-described, and we propose that the peptide(s) responsible for the striking ACE-mediated enhancement of myeloid function are substrates/products of the ACE C-domain.
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