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Sprouty2 regulates proliferation and survival of multiple myeloma by inhibiting activation of the ERK1/2 pathway in vitro and in vivo

Multiple myeloma (MM) is an incurable disease, and its pathogenesis remains unclear. MicroRNA (miR)-21 was detected at a high level in MM and plays a key role in the pathogenesis of MM. However, Sprouty2 (spry2), a downstream target of miR-21, has low expression, and its mechanism in MM is unknown.... Full description

Journal Title: Experimental Hematology June 2016, Vol.44(6), pp.474-482.e2
Main Author: Yao, Yao
Other Authors: Luo, Jianping , Bian, Yueping , Sun, Yueyue , Shi, Min , Xia, Dandan , Niu, Mingshan , Zhao, Kai , Zeng, Lingyu , Chen, Wei , Li, Zhenyu , Xu, Kailin
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0301-472X ; DOI: 10.1016/j.exphem.2016.02.009
Link: http://dx.doi.org/10.1016/j.exphem.2016.02.009
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recordid: sciversesciencedirect_elsevierS0301-472X(16)00073-4
title: Sprouty2 regulates proliferation and survival of multiple myeloma by inhibiting activation of the ERK1/2 pathway in vitro and in vivo
format: Article
creator:
  • Yao, Yao
  • Luo, Jianping
  • Bian, Yueping
  • Sun, Yueyue
  • Shi, Min
  • Xia, Dandan
  • Niu, Mingshan
  • Zhao, Kai
  • Zeng, Lingyu
  • Chen, Wei
  • Li, Zhenyu
  • Xu, Kailin
subjects:
  • Multiple Myeloma
  • Protein Kinases
  • Endothelial Growth Factors
  • Mitogens
ispartof: Experimental Hematology, June 2016, Vol.44(6), pp.474-482.e2
description: Multiple myeloma (MM) is an incurable disease, and its pathogenesis remains unclear. MicroRNA (miR)-21 was detected at a high level in MM and plays a key role in the pathogenesis of MM. However, Sprouty2 (spry2), a downstream target of miR-21, has low expression, and its mechanism in MM is unknown. We investigated whether spry2 could exert an antimyeloma effect and further studied the potential pathogenesis and progression of MM. To address the functional consequences of spry2, we assessed the expression levels of spry2 in several myeloma cell lines and detected low expression levels in MM cells. Overexpression of spry2 suppressed growth and colony formation ability and decreased the phosphorylation of extracellular signal-regulated kinases 1 and 2. Spry2 also decreased secretion of vascular endothelial growth factor and partially enhanced the sensitivity of MM cells to an inhibitor of mitogen-activated protein kinases 1 and 2. Additionally, spry2 inhibited the tumorigenesis and angiogenesis of MM cells in vivo. In summary, we report for the first time that spry2 can inhibit MM cell growth and survival with a concomitant reduction in phosphorylation of extracellular signal-regulated kinases 1 and 2 in vitro and in vivo. •Sprouty2 is expressed at low levels in multiple myeloma cells.•Overexpression of sprouty2 suppressed growth, colony formation ability, and activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2).•Overexpression of sprouty2 decreased secretion of vascular endothelial growth factor and enhanced the sensitivity of multiple myeloma cells to an inhibitor of mitogen-activated protein kinases 1 and 2 (MEK1/2).•Overexpression of sprouty2 inhibited the tumorigenesis of multiple myeloma cells in vivo.
language: eng
source:
identifier: ISSN: 0301-472X ; DOI: 10.1016/j.exphem.2016.02.009
fulltext: fulltext
issn:
  • 0301472X
  • 0301-472X
url: Link


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titleSprouty2 regulates proliferation and survival of multiple myeloma by inhibiting activation of the ERK1/2 pathway in vitro and in vivo
creatorYao, Yao ; Luo, Jianping ; Bian, Yueping ; Sun, Yueyue ; Shi, Min ; Xia, Dandan ; Niu, Mingshan ; Zhao, Kai ; Zeng, Lingyu ; Chen, Wei ; Li, Zhenyu ; Xu, Kailin
ispartofExperimental Hematology, June 2016, Vol.44(6), pp.474-482.e2
identifierISSN: 0301-472X ; DOI: 10.1016/j.exphem.2016.02.009
descriptionMultiple myeloma (MM) is an incurable disease, and its pathogenesis remains unclear. MicroRNA (miR)-21 was detected at a high level in MM and plays a key role in the pathogenesis of MM. However, Sprouty2 (spry2), a downstream target of miR-21, has low expression, and its mechanism in MM is unknown. We investigated whether spry2 could exert an antimyeloma effect and further studied the potential pathogenesis and progression of MM. To address the functional consequences of spry2, we assessed the expression levels of spry2 in several myeloma cell lines and detected low expression levels in MM cells. Overexpression of spry2 suppressed growth and colony formation ability and decreased the phosphorylation of extracellular signal-regulated kinases 1 and 2. Spry2 also decreased secretion of vascular endothelial growth factor and partially enhanced the sensitivity of MM cells to an inhibitor of mitogen-activated protein kinases 1 and 2. Additionally, spry2 inhibited the tumorigenesis and angiogenesis of MM cells in vivo. In summary, we report for the first time that spry2 can inhibit MM cell growth and survival with a concomitant reduction in phosphorylation of extracellular signal-regulated kinases 1 and 2 in vitro and in vivo. •Sprouty2 is expressed at low levels in multiple myeloma cells.•Overexpression of sprouty2 suppressed growth, colony formation ability, and activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2).•Overexpression of sprouty2 decreased secretion of vascular endothelial growth factor and enhanced the sensitivity of multiple myeloma cells to an inhibitor of mitogen-activated protein kinases 1 and 2 (MEK1/2).•Overexpression of sprouty2 inhibited the tumorigenesis of multiple myeloma cells in vivo.
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titleSprouty2 regulates proliferation and survival of multiple myeloma by inhibiting activation of the ERK1/2 pathway in vitro and in vivo
descriptionMultiple myeloma (MM) is an incurable disease, and its pathogenesis remains unclear. MicroRNA (miR)-21 was detected at a high level in MM and plays a key role in the pathogenesis of MM. However, Sprouty2 (spry2), a downstream target of miR-21, has low expression, and its mechanism in MM is unknown. We investigated whether spry2 could exert an antimyeloma effect and further studied the potential pathogenesis and progression of MM. To address the functional consequences of spry2, we assessed the expression levels of spry2 in several myeloma cell lines and detected low expression levels in MM cells. Overexpression of spry2 suppressed growth and colony formation ability and decreased the phosphorylation of extracellular signal-regulated kinases 1 and 2. Spry2 also decreased secretion of vascular endothelial growth factor and partially enhanced the sensitivity of MM cells to an inhibitor of mitogen-activated protein kinases 1 and 2. Additionally, spry2 inhibited the tumorigenesis and angiogenesis of MM cells in vivo. In summary, we report for the first time that spry2 can inhibit MM cell growth and survival with a concomitant reduction in phosphorylation of extracellular signal-regulated kinases 1 and 2 in vitro and in vivo. •Sprouty2 is expressed at low levels in multiple myeloma cells.•Overexpression of sprouty2 suppressed growth, colony formation ability, and activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2).•Overexpression of sprouty2 decreased secretion of vascular endothelial growth factor and enhanced the sensitivity of multiple myeloma cells to an inhibitor of mitogen-activated protein kinases 1 and 2 (MEK1/2).•Overexpression of sprouty2 inhibited the tumorigenesis of multiple myeloma cells in vivo.
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titleSprouty2 regulates proliferation and survival of multiple myeloma by inhibiting activation of the ERK1/2 pathway in vitro and in vivo
authorYao, Yao ; Luo, Jianping ; Bian, Yueping ; Sun, Yueyue ; Shi, Min ; Xia, Dandan ; Niu, Mingshan ; Zhao, Kai ; Zeng, Lingyu ; Chen, Wei ; Li, Zhenyu ; Xu, Kailin
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abstractMultiple myeloma (MM) is an incurable disease, and its pathogenesis remains unclear. MicroRNA (miR)-21 was detected at a high level in MM and plays a key role in the pathogenesis of MM. However, Sprouty2 (spry2), a downstream target of miR-21, has low expression, and its mechanism in MM is unknown. We investigated whether spry2 could exert an antimyeloma effect and further studied the potential pathogenesis and progression of MM. To address the functional consequences of spry2, we assessed the expression levels of spry2 in several myeloma cell lines and detected low expression levels in MM cells. Overexpression of spry2 suppressed growth and colony formation ability and decreased the phosphorylation of extracellular signal-regulated kinases 1 and 2. Spry2 also decreased secretion of vascular endothelial growth factor and partially enhanced the sensitivity of MM cells to an inhibitor of mitogen-activated protein kinases 1 and 2. Additionally, spry2 inhibited the tumorigenesis and angiogenesis of MM cells in vivo. In summary, we report for the first time that spry2 can inhibit MM cell growth and survival with a concomitant reduction in phosphorylation of extracellular signal-regulated kinases 1 and 2 in vitro and in vivo. •Sprouty2 is expressed at low levels in multiple myeloma cells.•Overexpression of sprouty2 suppressed growth, colony formation ability, and activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2).•Overexpression of sprouty2 decreased secretion of vascular endothelial growth factor and enhanced the sensitivity of multiple myeloma cells to an inhibitor of mitogen-activated protein kinases 1 and 2 (MEK1/2).•Overexpression of sprouty2 inhibited the tumorigenesis of multiple myeloma cells in vivo.
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