ArticleFrontiers in pharmacology2017
E-M, an Engineered Endostatin with High ATPase Activity, Inhibits the Recruitment and Alternative Activation of Macrophages in Non-small Cell Lung Cancer.
Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Tumor-associated macrophages within the immunological milieu: An emerging focal point for therapeutic intervention.Heliyon · 2024Review
- Beyond biomarkers: Exploring the diverse potential of a novel phosphoprotein in lung cancer management.Journal of cellular and molecular medicine · 2024Review
- [Tumor-associated Macrophage: Emerging Targets for Modulating the Tumor Microenvironment].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Review
- Recombinant Endostatin as a Potential Radiosensitizer in the Treatment of Non-Small Cell Lung Cancer.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Cancer immune exclusion: breaking the barricade for a successful immunotherapy.Frontiers in oncology · 2023Review
- Review
- ITGA5 is a prognostic biomarker and correlated with immune infiltration in gastrointestinal tumors.BMC cancer · 2021Article
- Prostate Epithelial RON Signaling Promotes M2 Macrophage Activation to Drive Prostate Tumor Growth and Progression.Molecular cancer research : MCR · 2020Article
- Dioscin elicits anti-tumour immunity by inhibiting macrophage M2 polarization via JNK and STAT3 pathways in lung cancer.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endostatin recently was reported by our laboratory to possess ATPase activity that is indispensable for its anti-angiogenesis and anti-tumor effects. An engineered endostatin, E-M, which owns higher ATPase activity exhibits stronger inhibitory effects on angiogenesis. Tumor-associated macrophages (TAMs), especially M2-polarized TAMs, contribute to tumor progression by promoting tumor cell proliferation, metastasis, angiogenesis, and immunosuppression, thus emerging as crucial targets for therapeutic intervention. Endostatin reportedly modulated functions of TAMs, but the detailed mechanisms remain unclear. Here, in our study, we demonstrated that E-M exhibited stronger inhibitory effects on macrophages than endostatin and other low ATPase mutants, which indicates that the ATPase activity is required for the inhibitory effects of endostatin on TAMs. Moreover, we elucidated that endostatin co-receptor, nucleolin and integrin α5β1, overexpressed on the surface of M2 macrophages, facilitated the internalization of E-M via the caveolae/lipid raft- and clathrin-dependent pathways. E-M inhibited the migration of TAMs through blockade of p38 MAP kinase and Erk1/2 signaling pathways, and prevented the alternative activation of TAMs. As a result, TAM-induced tumor cell proliferation and angiogenic activities
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