American Association for Cancer Research
00085472can120762-sup-tab1.pdf (91.35 kB)

Supplementary Table 1 from Neuropilin-1 Identifies a Subset of Bone Marrow Gr1− Monocytes That Can Induce Tumor Vessel Normalization and Inhibit Tumor Growth

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posted on 2023-03-30, 21:32 authored by Alessandro Carrer, Silvia Moimas, Serena Zacchigna, Lucia Pattarini, Lorena Zentilin, Giulia Ruozi, Miguel Mano, Milena Sinigaglia, Federica Maione, Guido Serini, Enrico Giraudo, Federico Bussolino, Mauro Giacca

PDF file - 91K, Supplementary Table 1. List of genes analyzed for expression by real-time, quantitative RT-PCR. All the amplifications were performed on a 7000 ABI Prism Instrument (Applied Biosystems), using pre-developed assays ("Mm" code), custom assays (for CCL5 and CXCR4) (Applied Biosystems) or SYBR Green (for Gr-1 and HPRT). The housekeeping genes GAPDH and HPRT were used to normalize the results.



Improving tumor perfusion, thus tempering tumor-associated hypoxia, is known to impair cancer progression. Previous work from our laboratory has shown that VEGF-A165 and semaphorin 3A (Sema3A) promote vessel maturation through the recruitment of a population of circulating monocytes expressing the neuropilin-1 (Nrp1) receptor (Nrp1-expressing monocytes; NEM). Here, we define the characteristics of bone marrow NEMs and assess whether these cells might represent an exploitable tool to induce tumor vessel maturation. Gene expression signature and surface marker analysis have indicated that NEMs represent a specific subset of CD11b+ Nrp1+ Gr1− resident monocytes, distinctively recruited by Sema3A. NEMs were found to produce several factors involved in vessel maturation, including PDGFb, TGF-β, thrombospondin-1, and CXCL10; consistently, they were chemoattractive for vascular smooth muscle cells in vitro. When directly injected into growing tumors, NEMs, isolated either from the bone marrow or from Sema3A-expressing muscles, exerted antitumor activity despite having no direct effects on the proliferation of tumor cells. NEM inoculation specifically promoted mural cell coverage of tumor vessels and decreased vascular leakiness. Tumors treated with NEMs were smaller, better perfused and less hypoxic, and had a reduced level of activation of HIF-1α. We conclude that NEMs represent a novel, unique population of myeloid cells that, once inoculated into a tumor, induce tumor vessel normalization and inhibit tumor growth. Cancer Res; 72(24); 6371–81. ©2012 AACR.

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