G-protein-coupled receptor agonist BV8/prokineticin-2 and STAT3 protein form a feed-forward loop in both normal and malignant myeloid cells

Hong Xin; Rongze Lu; Heehyoung Lee; Wang Zhang; Chunyan Zhang; Jiehui Deng; Yong Liu; Shudan Shen; Kay Uwe Wagner; Stephen Forman; Richard Jove; Hua Yu

doi:10.1074/jbc.M113.450049

G-protein-coupled receptor agonist BV8/prokineticin-2 and STAT3 protein form a feed-forward loop in both normal and malignant myeloid cells

Hong Xin, Rongze Lu, Heehyoung Lee, Wang Zhang, Chunyan Zhang, Jiehui Deng, Yong Liu, Shudan Shen, Kay Uwe Wagner, Stephen Forman, Richard Jove, Hua Yu

Research output: Contribution to journal › Article › peer-review

43 Scopus citations

Abstract

Background: Signaling pathways underlying BV8-mediated oncogenesis remain unknown. Results: BV8-STAT3 forms a feed-forward loop in both normal and malignant myeloid cells and promotes tumor growth. Conclusion: JAK2/STAT3 signaling plays critical roles in BV8-mediated myeloid cell-dependent oncogenesis. Significance: This study identifies a novel role of BV8-STAT3 signaling in mediating cross-talk between tumor microenvironment and tumor cells.

Original language	English (US)
Pages (from-to)	13842-13849
Number of pages	8
Journal	Journal of Biological Chemistry
Volume	288
Issue number	19
DOIs	https://doi.org/10.1074/jbc.M113.450049
State	Published - May 10 2013
Externally published	Yes

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Cell Biology

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title = "G-protein-coupled receptor agonist BV8/prokineticin-2 and STAT3 protein form a feed-forward loop in both normal and malignant myeloid cells",

abstract = "Background: Signaling pathways underlying BV8-mediated oncogenesis remain unknown. Results: BV8-STAT3 forms a feed-forward loop in both normal and malignant myeloid cells and promotes tumor growth. Conclusion: JAK2/STAT3 signaling plays critical roles in BV8-mediated myeloid cell-dependent oncogenesis. Significance: This study identifies a novel role of BV8-STAT3 signaling in mediating cross-talk between tumor microenvironment and tumor cells.",

author = "Hong Xin and Rongze Lu and Heehyoung Lee and Wang Zhang and Chunyan Zhang and Jiehui Deng and Yong Liu and Shudan Shen and Wagner, {Kay Uwe} and Stephen Forman and Richard Jove and Hua Yu",

year = "2013",

month = may,

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doi = "10.1074/jbc.M113.450049",

language = "English (US)",

volume = "288",

pages = "13842--13849",

journal = "Journal of Biological Chemistry",

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TY - JOUR

T1 - G-protein-coupled receptor agonist BV8/prokineticin-2 and STAT3 protein form a feed-forward loop in both normal and malignant myeloid cells

AU - Xin, Hong

AU - Lu, Rongze

AU - Lee, Heehyoung

AU - Zhang, Wang

AU - Zhang, Chunyan

AU - Deng, Jiehui

AU - Liu, Yong

AU - Shen, Shudan

AU - Wagner, Kay Uwe

AU - Forman, Stephen

AU - Jove, Richard

AU - Yu, Hua

PY - 2013/5/10

Y1 - 2013/5/10

N2 - Background: Signaling pathways underlying BV8-mediated oncogenesis remain unknown. Results: BV8-STAT3 forms a feed-forward loop in both normal and malignant myeloid cells and promotes tumor growth. Conclusion: JAK2/STAT3 signaling plays critical roles in BV8-mediated myeloid cell-dependent oncogenesis. Significance: This study identifies a novel role of BV8-STAT3 signaling in mediating cross-talk between tumor microenvironment and tumor cells.

AB - Background: Signaling pathways underlying BV8-mediated oncogenesis remain unknown. Results: BV8-STAT3 forms a feed-forward loop in both normal and malignant myeloid cells and promotes tumor growth. Conclusion: JAK2/STAT3 signaling plays critical roles in BV8-mediated myeloid cell-dependent oncogenesis. Significance: This study identifies a novel role of BV8-STAT3 signaling in mediating cross-talk between tumor microenvironment and tumor cells.

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DO - 10.1074/jbc.M113.450049

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AN - SCOPUS:84877718125

SN - 0021-9258

VL - 288

SP - 13842

EP - 13849

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

IS - 19

ER -

G-protein-coupled receptor agonist BV8/prokineticin-2 and STAT3 protein form a feed-forward loop in both normal and malignant myeloid cells

Abstract

ASJC Scopus subject areas

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