CXCR2 expression on granulocyte and macrophage progenitors under tumor conditions contributes to mo-MDSC generation via SAP18/ERK/STAT3.

Tytuł:: CXCR2 expression on granulocyte and macrophage progenitors under tumor conditions contributes to mo-MDSC generation via SAP18/ERK/STAT3.
Autorzy:: Han X; The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Shi H; People's Hospital of Rizhao, Rizhao, China.
Sun Y; The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Shang C; The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Luan T; The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Wang D; The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China.
Ba X; The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China. .
Zeng X; The Key Laboratory of Molecular Epigenetics of Ministry of Education, Institute of Genetics and Cytology, School of Life Science, Northeast Normal University, Changchun, Jilin, China. .
Źródło:: Cell death & disease [Cell Death Dis] 2019 Aug 08; Vol. 10 (8), pp. 598. Date of Electronic Publication: 2019 Aug 08.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Original Publication: London : Nature Pub. Group
MeSH Terms:: Co-Repressor Proteins/*genetics
Granulocyte-Macrophage Progenitor Cells/*metabolism
Melanoma, Experimental/*genetics
RNA-Binding Proteins/*genetics
Receptors, Interleukin-8B/*genetics
STAT3 Transcription Factor/*genetics
Animals ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic/genetics ; Granulocyte-Macrophage Progenitor Cells/pathology ; Humans ; MAP Kinase Signaling System/genetics ; Melanoma, Experimental/pathology ; Mice ; Monocytes/metabolism ; Monocytes/pathology ; Myeloid-Derived Suppressor Cells/metabolism ; Myeloid-Derived Suppressor Cells/pathology ; RNA, Small Interfering/pharmacology ; Receptors, Interleukin-8B/antagonists & inhibitors ; Tumor Microenvironment/genetics
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Substance Nomenclature:: 0 (Co-Repressor Proteins)
0 (Cxcr2 protein, mouse)
0 (RNA, Small Interfering)
0 (RNA-Binding Proteins)
0 (Receptors, Interleukin-8B)
0 (STAT3 Transcription Factor)
0 (Sap18 protein, mouse)
0 (Stat3 protein, mouse)
Entry Date(s):: Date Created: 20190810 Date Completed: 20200730 Latest Revision: 20200730
Update Code:: 20240104
PubMed Central ID:: PMC6687752
DOI:: 10.1038/s41419-019-1837-1
PMID:: 31395859
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Myeloid-derived suppressor cells (MDSCs) comprise a critical component of the tumor environment and CXCR2 reportedly plays a key role in the pathophysiology of various inflammatory diseases. Here, CXCR2 expression on granulocyte and macrophage progenitor cells (GMPs) was found to participate in myeloid cell differentiation within the tumor environment. In CXCR2-deficient tumor-bearing mice, GMPs exhibited fewer macrophage and dendritic cell progenitor cells than wild-type tumor-bearing mice, thereby decreasing monocytic MDSCs (mo-MDSCs) expansion. CXCR2 deficiency increased SAP18 expression in tumor-bearing mice, which reduced STAT3 phosphorylation through restraining ERK1/2 activation. Our findings reveal a critical role for CXCR2 in regulating hematopoietic progenitor cell differentiation under tumor conditions, and SAP18 is a key negative regulator in this process. Thus, inhibiting CXCR2 expression may alter the tumor microenvironment and attenuate tumor progression.

Erratum in: Cell Death Dis. 2019 Sep 5;10(9):641. (PMID: 31488810)

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