Human chorionic gonadotropin β induces migration and invasion via activating ERK1/2 and MMP-2 in human prostate cancer DU145 cells

PLoS One. 2013;8(2):e54592. doi: 10.1371/journal.pone.0054592. Epub 2013 Feb 12.

Abstract

We previously demonstrated that human chorionic gonadotropin β (hCGβ) induced migration and invasion in human prostate cancer cells. However, the involved molecular mechanisms are unclear. Here, we established a stable prostate cancer cell line overexpressing hCGβ and tested hCGβ-triggered signaling pathways causing cell migration and invasion. ELISA showed that the hCGβ amount secreted into medium increased with culture time after the hCGβ-transfected cells were incubated for 3, 6, 9, 12 and 24 h. More, hCGβ standards promoted MAPK (ERK1/2) phosphorylation and increased MMP-2 expression and activity in both dose- and time-dependent manners in hCGβ non-transfected cells. In addition, hCGβ promoted ERK1/2 phosphorylation and increased MMP-2 expression and activity significantly in hCGβ transfected DU145 cells. Whereas ERK1/2 blocker PD98059 (25 µM) significantly downregulated phosphorylated ERK1/2 and MMP-2. Particularly, hCGβ promoted cell migration and invasion, yet the PD98059 diminished the hCGβ-induced cell motility under those conditions. These results indicated that hCGβ induced cell motility via promoting ERK1/2 phosphorylation and MMP-2 upregulation in human prostate cancer DU145 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Cell Movement*
  • Chorionic Gonadotropin, beta Subunit, Human / genetics
  • Chorionic Gonadotropin, beta Subunit, Human / metabolism*
  • Enzyme Activation
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Matrix Metalloproteinase 2 / metabolism*
  • Mitogen-Activated Protein Kinase 1 / metabolism*
  • Mitogen-Activated Protein Kinase 3 / metabolism*
  • Neoplasm Invasiveness
  • Phosphorylation
  • Prostatic Neoplasms / pathology*
  • Signal Transduction

Substances

  • Chorionic Gonadotropin, beta Subunit, Human
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Matrix Metalloproteinase 2

Grants and funding

This study was funded by Science and Development Plan of Beijing Education Committee (grant number: KM200910025008) and National Natural Science Foundation of China (grant number: 81272843). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.