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Chinese Archives of General Surgery(Electronic Edition) ›› 2020, Vol. 14 ›› Issue (06): 406-410. doi: 10.3877/cma.j.issn.1674-0793.2020.06.002

Special Issue:

• Original Article • Previous Articles     Next Articles

Investigation of miR-223 in regulating breast cancer cells and osteoclast function via IGF-1R and NFIA

Zhen Shan1, Wen Li2, Yuanjian Fan1, Zefei Lin2, Ying Lin1, Shenming Wang1,()   

  1. 1. Department of Thyroid and Breast Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China
    2. Laboratory of General Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China
  • Received:2020-09-10 Online:2020-12-01 Published:2020-12-01
  • Contact: Shenming Wang
  • About author:
    Corresponding author: Wang Shenming, Email:

Abstract:

Objective

To investigate the effect and mechanism of miR-223 in regulating breast cancer cells and osteoclast in bone metastasis microenvironment.

Methods

The role of miR-223 in regulating bone resorption was evaluated by micro-CT and histologic section in miR-223 knockout and C57BL/6 mice. The effect and mechanism of miR-223 in RANKL induced osteoclast formation was investigated. The role and mechanism of miR-223 in regulating breast cancer cell proliferation and apoptosis were investigated in MDA-MB-231 cell line.

Results

The osteoclastic resorption was more severe inmiR-223 knockout mice. In vitro, miR-223 could suppress RANKL activating osteocalst formation by targeting NFIA protein. Besides, overexpression of miR-223 inhibited MDA-MB-231 cell proliferation and promoted its apoptosis by targeting IGF-1R and PI3K/Akt pathway.

Conclusion

miR-223 is a protective factor in bone metastasis microenvironment, which can suppress bone resorption by inhibiting osteoclast formation, and suppress breast cancer cell proliferation, enhance breast cancer cell apoptosis.

Key words: Breast neoplasms, MicroRNAs, Bone metastasi, Osteoclasts

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