Oncotarget

Research Papers:

MiR-507 inhibits the migration and invasion of human breastcancer cells through Flt-1 suppression

Liyan Jia, Wei Liu, Bo Cao, Hongli Li and Chonggao Yin _

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Oncotarget. 2016; 7:36743-36754. https://doi.org/10.18632/oncotarget.9163

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Abstract

Liyan Jia1,*, Wei Liu1,*, Bo Cao1, Hongli Li2, Chonggao Yin3

1Affiliated Hospital, Weifang Medical University, Weifang, 261053, China

2Medicine Research Center, Weifang Medical University, Weifang, 261053, China

3College of Nursing, Weifang Medical University, Weifang, 261053, China

*These authors have contributed equally to this work

Correspondence to:

Chonggao Yin, email: [email protected], [email protected]

Hongli Li, email: [email protected]

Keywords: miR-507, Flt-1, molecular mechanism, invasion, PlGF-1

Received: February 14, 2016     Accepted: April 16, 2016     Published: May 4, 2016

ABSTRACT

Vascular endothelial growth factor receptor-1/fms-related tyrosine kinase-1 (VEGFR-1/Flt-1) is a tyrosine kinase receptor that binds placental growth factor (PlGF). Flt-1 is also highly expressed in breast-cancer tissues and breast-cancer cell lines. However, the molecular mechanism by which Flt-1 promotes breast-cancer invasion and metastasis by binding to PlGF-1 is unclear. In this study, we discovered that PlGF-1 and Flt-1 played a key role in the migration and invasion of breast cancer. Flt-1 promoted the migration and chemotaxis of breast-cancer cells by binding to PlGF-1. In addition, Flt-1 was confirmed to be a direct target gene of miR-507. miR-507 up-regulation inhibited the invasion and metastasis of breast-cancer cells in vitro and in vivo. Flt-1 overexpression rescued the invasion partially caused by the ectopic expression of miR-507. miR-507 expression in breast-cancer tissues and cell lines was lower than that in adjacent non-neoplastic tissues and normal cells. Clinical analysis indicated that miR-507 was negatively correlated with tumor differentiation, lymphatic metastasis, and the expression of Flt-1 in breast cancer. Furthermore, we showed that miR-507 down-regulation was due to the hypermethylation of its promotor region. Our results indicated that miR-507 represented potential therapeutic targets in breast cancer by modulating Flt-1.


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