Increased expression of preprotachykinin-I and neurokinin receptors in human breast cancer cells: implications for bone marrow metastasis

Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):388-93. doi: 10.1073/pnas.97.1.388.

Abstract

Neuropeptides are implicated in many tumors, breast cancer (BC) included. Preprotachykinin-I (PPT-I) encodes multiple neuropeptides with pleiotropic functions such as neurotransmission, immune/hematopoietic modulation, angiogenesis, and mitogenesis. PPT-I is constitutively expressed in some tumors. In this study, we investigated a role for PPT-I and its receptors, neurokinin-1 (NK-1) and NK-2, in BC by using quantitative reverse transcription-PCR, ELISA, and in situ hybridization. Compared with normal mammary epithelial cells (n = 2) and benign breast biopsies (n = 21), BC cell lines (n = 7) and malignant breast biopsies (n = 25) showed increased expression of PPT-I and NK-1. NK-2 levels were high in normal and malignant cells. Specific NK-1 and NK-2 antagonists inhibited BC cell proliferation, suggesting autocrine and/or intercrine stimulation of BC cells by PPT-I peptides. NK-2 showed no effect on the proliferation of normal cells but mediated the proliferation of BC cells. Cytosolic extracts from malignant BC cells enhanced PPT-I translation whereas extracts from normal mammary epithelial cells caused no change. These enhancing effects may be protein-specific because a similar increase was observed for IL-6 translation and no effect was observed for IL-1alpha and stem cell factor. The data suggest that PPT-I peptides and their receptors may be important in BC development. Considering that PPT-I peptides are hematopoietic modulators, these results could be extended to understand early integration of BC cells in the bone marrow, a preferred site of metastasis. Molecular signaling transduced by PPT-I peptides and the mechanism that enhances translation of PPT-I mRNA could lead to innovative strategies for BC treatments and metastasis.

Publication types

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

MeSH terms

  • Benzamides / pharmacology
  • Biphenyl Compounds / pharmacology
  • Bone Marrow Cells
  • Bone Marrow Neoplasms / secondary*
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / therapy
  • Cell Division / drug effects
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Humans
  • In Situ Hybridization
  • Neurokinin-1 Receptor Antagonists
  • Piperidines / pharmacology
  • Protein Precursors / genetics*
  • Protein Precursors / metabolism
  • Receptors, Neurokinin-1 / genetics*
  • Receptors, Neurokinin-2 / antagonists & inhibitors
  • Receptors, Neurokinin-2 / genetics*
  • Substance P / antagonists & inhibitors
  • Substance P / metabolism
  • Tachykinins / genetics*
  • Tachykinins / metabolism
  • Tumor Cells, Cultured

Substances

  • Benzamides
  • Biphenyl Compounds
  • Neurokinin-1 Receptor Antagonists
  • Piperidines
  • Protein Precursors
  • Receptors, Neurokinin-1
  • Receptors, Neurokinin-2
  • Tachykinins
  • preprotachykinin
  • Substance P
  • SR 48968
  • CP 96345