4.1 Article

Estradiol-Induced MMP-9 Expression via PELP1-Mediated Membrane-Initiated Signaling in ERα-Positive Breast Cancer Cells

Journal

HORMONES & CANCER
Volume 11, Issue 2, Pages 87-96

Publisher

SPRINGER
DOI: 10.1007/s12672-020-00380-8

Keywords

Proline-; glutamic acid-; leucine-rich protein 1; Matrix metalloproteinase-9; Estrogen; Breast cancer

Funding

  1. Fundamental Research Funds for the Provincial Universities [JFXN201906, JFXN201910]
  2. Scientific Research Fund of Harbin Medical University-Daqing [DQ2013-1]
  3. Postgraduate Tutor Foundation of Harbin Medical University-Daqing [DSJJ2015003]

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Proline-, glutamic acid-, leucine-rich protein 1 (PELP1) is a novel estrogen receptor (ER) coregulator, demonstrated distinctive characters from other ER alpha coregulators, and has been suggested to be involved in metastasis of several cancers. In ER alpha-positive breast cancer, PELP1 overexpression enhanced ruffles and filopodium-like structure stimulated by estradiol (E-2) through extranuclear cell signaling transduction hereby increased cell motility. However, whether PELP1 is also involved in extracellular matrix remodeling of ER alpha-positive breast cancer cells is still unknown. In this study, we investigated the role of PELP1 in E-2-induced MMP-9 expression and the underlined mechanism. The results demonstrated the following: E-2-induced ER alpha-positive MCF-7 breast cancer cell MMP-9 mRNA and protein expression in a rapid response and concentration-dependent manner. Knocked down PELP1 significantly suppressed E-2-induced MMP-9 expression. E-2-bovine serum albumin (BSA), a large molecular membrane-impenetrable conjugate of E-2, can also upregulate MMP-9 protein expression in MCF-7, and the action of E-2-BSA can be abolished by PI3K inhibitor LY294002; treating MCF-7 simultaneously with PELP1-shRNA and LY294002 did not show synergetic inhibitory effect on E-2-BSA-induced MMP-9 expression. Our results indicated that estrogen-induced MMP-9 expression in ER-positive breast cancer cells may be through PELP1-mediated PI3K/Akt signaling pathway.

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