Impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma

Aim: To evaluate the role of endostatin (ES) gene therapy on myeloid-derived suppressor cells (MDSC) in a metastatic model of renal cell carcinoma (RCC). Materials and Methods: Balb/C mice bearing orthotopic Renca tumors were treated with NIH/3T3LendSN or, as a control, with NIH/3T3-LXSN cells. At t...

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Опубліковано в: :Experimental Oncology
Дата:2018
Автори: Chaves, K.C.B., Costa, E.M., Teixeira, L.F., Bellini, M.H.
Формат: Стаття
Мова:Англійська
Опубліковано: Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України 2018
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Онлайн доступ:https://nasplib.isofts.kiev.ua/handle/123456789/139248
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Назва журналу:Digital Library of Periodicals of National Academy of Sciences of Ukraine
Цитувати:Impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma / K.C.B. Chaves, E.M. Costa, L.F. Teixeira, M.H. Bellini // Experimental Oncology. — 2018 — Т. 40, № 1. — С. 24–32. — Бібліогр.: 48 назв. — англ.

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Digital Library of Periodicals of National Academy of Sciences of Ukraine
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author Chaves, K.C.B.
Costa, E.M.
Teixeira, L.F.
Bellini, M.H.
author_facet Chaves, K.C.B.
Costa, E.M.
Teixeira, L.F.
Bellini, M.H.
citation_txt Impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma / K.C.B. Chaves, E.M. Costa, L.F. Teixeira, M.H. Bellini // Experimental Oncology. — 2018 — Т. 40, № 1. — С. 24–32. — Бібліогр.: 48 назв. — англ.
collection DSpace DC
container_title Experimental Oncology
description Aim: To evaluate the role of endostatin (ES) gene therapy on myeloid-derived suppressor cells (MDSC) in a metastatic model of renal cell carcinoma (RCC). Materials and Methods: Balb/C mice bearing orthotopic Renca tumors were treated with NIH/3T3LendSN or, as a control, with NIH/3T3-LXSN cells. At the end of in vivo experiment, plasma and tissue lung samples were collected. Plasma ES and granulocyte colony stimulating factor (G-CSF) levels were measured by ELISA and Milliplex, respectively. Quantification of CD11b⁺Gr⁻1⁺ cells and their subsets was performed by flow cytometry. Reactive oxygen species (ROS) production was measured in CD11b⁺Gr⁻1⁺ MDSC using the DCFDA marker by flow cytometry. Results: Metastatic RCC (mRCC) induced expansions of CD11b⁺Gr⁻1⁺ MDSC and promoted accumulation of these cells and their subtypes in lymphoid organ and metastases. ES treatment promoted low G-CSF plasmatic levels which were produced by the tumor microenvironment, reflecting the reduced metastatic accumulation of CD11b⁺Gr⁻1⁺ MDSC in the lungs. However, the therapy was selective for granulocytic cells, thus reducing the production of ROS. Conclusion: These findings confirm the expansion of MDSC during metastatic progression of RCC and indicate the important role of ES in reducing MDSC and possible use of ES therapy in combined anticancer treatment.
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publisher Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України
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spelling Chaves, K.C.B.
Costa, E.M.
Teixeira, L.F.
Bellini, M.H.
2018-06-19T21:06:08Z
2018-06-19T21:06:08Z
2018
Impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma / K.C.B. Chaves, E.M. Costa, L.F. Teixeira, M.H. Bellini // Experimental Oncology. — 2018 — Т. 40, № 1. — С. 24–32. — Бібліогр.: 48 назв. — англ.
1812-9269
https://nasplib.isofts.kiev.ua/handle/123456789/139248
Aim: To evaluate the role of endostatin (ES) gene therapy on myeloid-derived suppressor cells (MDSC) in a metastatic model of renal cell carcinoma (RCC). Materials and Methods: Balb/C mice bearing orthotopic Renca tumors were treated with NIH/3T3LendSN or, as a control, with NIH/3T3-LXSN cells. At the end of in vivo experiment, plasma and tissue lung samples were collected. Plasma ES and granulocyte colony stimulating factor (G-CSF) levels were measured by ELISA and Milliplex, respectively. Quantification of CD11b⁺Gr⁻1⁺ cells and their subsets was performed by flow cytometry. Reactive oxygen species (ROS) production was measured in CD11b⁺Gr⁻1⁺ MDSC using the DCFDA marker by flow cytometry. Results: Metastatic RCC (mRCC) induced expansions of CD11b⁺Gr⁻1⁺ MDSC and promoted accumulation of these cells and their subtypes in lymphoid organ and metastases. ES treatment promoted low G-CSF plasmatic levels which were produced by the tumor microenvironment, reflecting the reduced metastatic accumulation of CD11b⁺Gr⁻1⁺ MDSC in the lungs. However, the therapy was selective for granulocytic cells, thus reducing the production of ROS. Conclusion: These findings confirm the expansion of MDSC during metastatic progression of RCC and indicate the important role of ES in reducing MDSC and possible use of ES therapy in combined anticancer treatment.
This study was supported by FAPESP (process: 2012/12955-2).
en
Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України
Experimental Oncology
Original contributions
Impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma
Article
published earlier
spellingShingle Impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma
Chaves, K.C.B.
Costa, E.M.
Teixeira, L.F.
Bellini, M.H.
Original contributions
title Impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma
title_full Impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma
title_fullStr Impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma
title_full_unstemmed Impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma
title_short Impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma
title_sort impact of endostatin gene therapy on myeloid-derived suppressor cells from a metastatic renal cell carcinoma
topic Original contributions
topic_facet Original contributions
url https://nasplib.isofts.kiev.ua/handle/123456789/139248
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