C-MYC-regulated miR-23a/24-2/27a cluster promotes mammary carcinoma cell invasion and hepatic metastasis by targeting sprouty2

Xiaoni Li; Xin Liu; Weiyi Xu; Peng Zhou; Ping Gao; Songshan Jiang; Peter E. Lobie; Tao Zhu

doi:10.1074/jbc.M113.478560

C-MYC-regulated miR-23a/24-2/27a cluster promotes mammary carcinoma cell invasion and hepatic metastasis by targeting sprouty2

Xiaoni Li, Xin Liu, Weiyi Xu, Peng Zhou, Ping Gao, Songshan Jiang, Peter E. Lobie, Tao Zhu

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

109 Scopus citations

Abstract

Background: The regulation of the miR-23a/24-2/27a cluster is largely unknown. Results: EGF induced c-MYC expression to promote the expression of the miR-23a/24-2/27a cluster, resulting in decreased expression of Sprouty2 and increased activation of p44/42 MAPK to stimulate mammary carcinoma cell invasion and subsequent hepatic metastases. Conclusion: EGF promoted mammary carcinoma cell invasion and hepatic metastasis. Significance: The miR-23a/24-2/27a cluster might be used as a biomarker for breast cancer metastasis.

Original language	English (US)
Pages (from-to)	18121-18133
Number of pages	13
Journal	Journal of Biological Chemistry
Volume	288
Issue number	25
DOIs	https://doi.org/10.1074/jbc.M113.478560
State	Published - Jun 21 2013
Externally published	Yes

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Cell Biology

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title = "C-MYC-regulated miR-23a/24-2/27a cluster promotes mammary carcinoma cell invasion and hepatic metastasis by targeting sprouty2",

abstract = "Background: The regulation of the miR-23a/24-2/27a cluster is largely unknown. Results: EGF induced c-MYC expression to promote the expression of the miR-23a/24-2/27a cluster, resulting in decreased expression of Sprouty2 and increased activation of p44/42 MAPK to stimulate mammary carcinoma cell invasion and subsequent hepatic metastases. Conclusion: EGF promoted mammary carcinoma cell invasion and hepatic metastasis. Significance: The miR-23a/24-2/27a cluster might be used as a biomarker for breast cancer metastasis.",

author = "Xiaoni Li and Xin Liu and Weiyi Xu and Peng Zhou and Ping Gao and Songshan Jiang and Lobie, {Peter E.} and Tao Zhu",

year = "2013",

month = jun,

day = "21",

doi = "10.1074/jbc.M113.478560",

language = "English (US)",

volume = "288",

pages = "18121--18133",

journal = "Journal of Biological Chemistry",

issn = "0021-9258",

publisher = "American Society for Biochemistry and Molecular Biology Inc.",

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TY - JOUR

T1 - C-MYC-regulated miR-23a/24-2/27a cluster promotes mammary carcinoma cell invasion and hepatic metastasis by targeting sprouty2

AU - Li, Xiaoni

AU - Liu, Xin

AU - Xu, Weiyi

AU - Zhou, Peng

AU - Gao, Ping

AU - Jiang, Songshan

AU - Lobie, Peter E.

AU - Zhu, Tao

PY - 2013/6/21

Y1 - 2013/6/21

N2 - Background: The regulation of the miR-23a/24-2/27a cluster is largely unknown. Results: EGF induced c-MYC expression to promote the expression of the miR-23a/24-2/27a cluster, resulting in decreased expression of Sprouty2 and increased activation of p44/42 MAPK to stimulate mammary carcinoma cell invasion and subsequent hepatic metastases. Conclusion: EGF promoted mammary carcinoma cell invasion and hepatic metastasis. Significance: The miR-23a/24-2/27a cluster might be used as a biomarker for breast cancer metastasis.

AB - Background: The regulation of the miR-23a/24-2/27a cluster is largely unknown. Results: EGF induced c-MYC expression to promote the expression of the miR-23a/24-2/27a cluster, resulting in decreased expression of Sprouty2 and increased activation of p44/42 MAPK to stimulate mammary carcinoma cell invasion and subsequent hepatic metastases. Conclusion: EGF promoted mammary carcinoma cell invasion and hepatic metastasis. Significance: The miR-23a/24-2/27a cluster might be used as a biomarker for breast cancer metastasis.

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JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

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C-MYC-regulated miR-23a/24-2/27a cluster promotes mammary carcinoma cell invasion and hepatic metastasis by targeting sprouty2

Abstract

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