HRG inhibits tumor growth and metastasis by inducing macrophage polarization and vessel normalization through downregulation of PlGF.

By Charlotte Rolny, M. Mazzone, Sonia Tugues, Damya Laoui, I. Johansson, Cathy Coulon, M. Squadrito, I. Segura, Xiujuan Li, Ellen Knevels and 17 more. Cancer Cell, 2011

705 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4eb1f5e85831f1d5017935816492cb09d1968510

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Citations in the corpus

Vascular normalizing doses of antiangiogenic treatment reprogram the immunosuppressive tumor microenvironment and enhance immunotherapy (2012, background): “Within breast cancer lesions, TAMs represent the dominant myeloid cell population and usually have an immunosuppressiveM2-like phenotype associated with the hypoxic tumor microenvironment (14, 17, 18).”
Basic and therapeutic aspects of angiogenesis. (2011, neutral): “Tumor-associated macrophages, especially those polarized to a proangiogenic M2-like phenotype, stimulate angiogenesis by releasing PlGF that also contributes to vessel disorganization (Grivennikov et al., 2010; Qian and Pollard, 2010; Rolny et al., 2011).”
The interaction of anticancer therapies with tumor-associated macrophages (2015, background): “In mice, HRG promoted antitumor immune responses and normalization of the vessel network (Rolny et al., 2011).”
Metastatic Stem Cells: Sources, Niches, and Vital Pathways (2014, background): “blood platelets (Bos et al., 2009; Chabottaux et al., 2009; Chen et al., 2011a; Gay and Felding-Habermann, 2011; Gocheva et al., 2010; Greenberg et al., 2008; Gupta et al., 2007; Kim et al., 2009; Labelle et al., 2011; Li et al., 2010; Padua et al., 2008; Reymond et al., 2013; Rolny et al., 2011; So”
Differential Macrophage Programming in the Tumor Microenvironment (2012, neutral): “Similarly, the TAM production of placental growth factor (PIGF), a homologue of VEGFA that selectively binds VEGF receptor 1 (VEGFR1), also stimulates angiogenesis in tumors [40] and may in part explain resistance to VEGFA and VEGFR targeted therapies in the clinic [41–43].”
Accessories to the crime: functions of cells recruited to the tumor microenvironment. (2012, neutral): “Similarly, TAM production of the VEGF family member PIGF stimulates angiogenesis in some tumors (Rolny et al., 2011) and thus TAMs may present a mechanism for acquiring resistance to anti-VEGF-A/VEGFR therapies (Fischer et al., 2007; Motzer et al., 2006; Willett et al., 2005).”
Low-dose irradiation programs macrophage differentiation to an iNOS⁺/M1 phenotype that orchestrates effective T cell immunotherapy. (2013, background): “M1 macrophages have been described to promote TH1 responses, support vascular normalization (Rolny et al., 2011), improve T cell recruitment (Johansson et al.”
Principles and mechanisms of vessel normalization for cancer and other angiogenic diseases (2011, background): “Stromal loss of PlGF improves the formation of an endothelial phalanx monolayer and vessel maturation, while reducing vessel leakage and remodelling; these changes increase tumour oxygenation and responses to chemotherap”
Vascular normalization as an emerging strategy to enhance cancer immunotherapy (2013, positive): “In keeping with this phenotype, HRG overexpression augmented DCs and CD8þ T-cell tumor infiltration and polarized TAMs away from an M2-like phenotype (28).”
Leukocyte Complexity Predicts Breast Cancer Survival and Functionally Regulates Response to Chemotherapy (2011, background): “6), it seems reasonable to speculate that TAM depletion resulted in loss of an important epithelial cell survival pathway (possibly mediated by EGF) that resists chemotherapy-induced cell death; certainly, however, effects on vascular pathways may also play a role, as has been recently reported by R”
Macrophage Polarization in Inflammatory Diseases (2014, background): “A recent study indicated that histidine-rich glycoprotein (HRG) could induce macrophage polarization and vessel normalization through the down-regulation of placental growth factor (PlGF), and inhibition of tumor growth as well as metastasis [82].”