Dual mechanisms for lysophospholipid induction of proliferation of human breast carcinoma cells

Cancer Res. 1999 Sep 15;59(18):4732-7.

Abstract

Endothelial differentiation gene-encoded G protein-coupled receptors (Edg Rs) Edg-1, Edg-3, and Edg-5 bind sphingosine 1-phosphate (S1P), and Edg-2 and Edg-4 Rs bind lysophosphatidic acid (LPA). LPA and S1P initiate ras- and rho-dependent signaling of cellular growth. Cultured lines of human breast cancer cells (BCCs) express Edg-3 > Edg-4 > Edg-5 > or = Edg-2, without detectable Edg-1, by both assessment of mRNA and Western blots with rabbit and monoclonal mouse anti-Edg R antibodies. BCC proliferation was stimulated significantly by 10(-9) M to 10(-6) M LPA and S1P. Luciferase constructs containing the serum response element (SRE) of growth-related gene promoters reported mean activation of BCCs by LPA and S1P of up to 85-fold. LPA and S1P stimulated BCC secretion of type II insulin-like growth factor (IGF-II) by 2-7-fold, to levels at which exogenous IGF-II stimulated increased proliferation and SRE activation of BCCs. All BCC responses to LPA and S1P were suppressed similarly by pertussis toxin, mitogen-activated protein kinase kinase inhibitors, and C3 exoenzyme inactivation of rho, suggesting mediation by Edg Rs. Monoclonal anti-IGF-II and anti-IGFR1 antibodies suppressed proliferation and SRE reports of BCCs to LPA and S1P by means of up to 65%. Edg Rs thus transduce LPA and S1P enhancement of BCC growth, both directly through SRE and indirectly by enhancing the contribution of IGF-II.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies / pharmacology
  • Antibodies, Monoclonal / pharmacology
  • Breast Neoplasms
  • Cell Division / drug effects*
  • DNA-Binding Proteins / analysis
  • DNA-Binding Proteins / genetics*
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • I-kappa B Proteins*
  • Immediate-Early Proteins / analysis
  • Immediate-Early Proteins / genetics*
  • Lysophospholipids / pharmacology*
  • Mice
  • NF-KappaB Inhibitor alpha
  • Nuclear Proteins / analysis
  • Nuclear Proteins / genetics*
  • RNA, Messenger / genetics
  • Rabbits
  • Receptors, Cell Surface / analysis
  • Receptors, Cell Surface / genetics*
  • Receptors, G-Protein-Coupled*
  • Receptors, Lysophosphatidic Acid
  • Receptors, Lysophospholipid
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sphingosine / analogs & derivatives
  • Sphingosine / pharmacokinetics
  • Sphingosine / pharmacology
  • Transcription Factors / analysis
  • Transcription Factors / genetics*
  • Transcription, Genetic / drug effects
  • Tumor Cells, Cultured

Substances

  • Antibodies
  • Antibodies, Monoclonal
  • DNA-Binding Proteins
  • I-kappa B Proteins
  • Immediate-Early Proteins
  • Lysophospholipids
  • NFKBIA protein, human
  • Nfkbia protein, mouse
  • Nuclear Proteins
  • RNA, Messenger
  • Receptors, Cell Surface
  • Receptors, G-Protein-Coupled
  • Receptors, Lysophosphatidic Acid
  • Receptors, Lysophospholipid
  • Transcription Factors
  • NF-KappaB Inhibitor alpha
  • sphingosine 1-phosphate
  • Sphingosine