Interactions Between Disseminated Tumor Cells and Bone Marrow Stromal Cells Regulate Tumor Dormancy

Curr Osteoporos Rep. 2018 Oct;16(5):596-602. doi: 10.1007/s11914-018-0471-7.

Abstract

Purpose of review: To succinctly summarize recent findings concerning dormancy regulating interactions between bone marrow stromal cells and disseminated tumor cells.

Recent findings: Recent studies have highlighted roles of the bone marrow microenviroment, including osteoblasts, mesenchymal stem cells (MSCs), and endothelial cells, in inducing or maintaining cancer cell dormancy. Key pathways of interest include: osteoblast-induced transforming growth factor (TGF)-β2 signaling, transfer of MSC-derived exosomes containing dormancy inducing microRNA, cancer cell cannibalism of MSCs, and endothelial cell secretion of thrombospondin 1 (TSP1). The bone marrow is a common site of metastatic disease recurrence following a period of cancer cell dormancy. Understanding why disseminated tumor cells enter into dormancy and later resume cell proliferation and growth is vital to developing effective therapeutics against these cells. The bone marrow stroma and the various pathways through which it participates in crosstalk with cancer cells are essential to furthering understanding of how dormancy is regulated.

Keywords: Bone marrow microenviroment; Bone marrow stromal cells; Cancer cell dormancy; Endothelial cells; Mesenchymal stem cells; Osteoblasts.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Cell Proliferation
  • Endothelial Cells / metabolism*
  • Exosomes / metabolism
  • Humans
  • Mesenchymal Stem Cells / metabolism*
  • MicroRNAs / metabolism
  • Neoplasms / metabolism*
  • Osteoblasts / metabolism*
  • Signal Transduction
  • Thrombospondin 1 / metabolism
  • Transforming Growth Factor beta2 / metabolism

Substances

  • MicroRNAs
  • Thrombospondin 1
  • Transforming Growth Factor beta2