Osteoclasts direct bystander killing of bone cancer

Cancer Res. 2006 Nov 15;66(22):10929-35. doi: 10.1158/0008-5472.CAN-06-1295.

Abstract

Primary and metastatic bone cancers are difficult to eradicate and novel approaches are needed to improve treatment and extend life. As bone cancer grows, osteoclasts, the principal bone-resorbing cells of the body, are recruited to and activated at sites of cancer. In this investigation, we determined if osteoclast lineage cells could function as a cell-based gene delivery system to bone cancers. We used the cytosine deaminase (CD) 5-fluorocytosine (5-FC) enzyme/prodrug system and studied bone marrow and bones from transgenic mice expressing a novel CD gene regulated by the osteoclast tartrate-resistant acid phosphatase (TRAP) gene promoter (Tg/NCD). DsRed2-labeled 2472 sarcoma cells were placed in Tg/NCD osteoclastogenic cultures and treated with 5-FC. 5-FC treatment resulted in profound bystander killing (90%; P < 0.05). The effect of 5-FC treatment on osteoclast lineage cells was most dramatic when administered at the beginning of the 7-day cultures, suggesting that mature osteoclasts are less sensitive to 5-FC. Evaluation of osteoclast-directed bystander killing in vivo revealed dramatic killing of bone cancer with only a modest effect on osteoclast number. Specifically, 5-FC treatment of tumor-bearing Tg/NCD mice or Tg/NCD bone marrow transplanted C3H mice (Tg/NCD-C3H) resulted in 92% and 44% reductions in tumor area, respectively (P < 0.05). Eight of ten 5-FC-treated Tg/NCD mice had complete bone tumor killing and five of six 5-FC-treated Tg/NCD-C3H mice had reduced tumor compared with controls. In addition, Tg/NCD osteoclasts were resistant to 5-FC treatment in vivo, a very important feature, as it identifies osteoclasts as an ideal CD gene delivery system.

Publication types

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

MeSH terms

  • Acid Phosphatase / genetics
  • Animals
  • Antimetabolites, Antineoplastic / pharmacokinetics
  • Antimetabolites, Antineoplastic / pharmacology
  • Bone Neoplasms / genetics
  • Bone Neoplasms / metabolism
  • Bone Neoplasms / pathology*
  • Bone Neoplasms / therapy*
  • Cell Line, Tumor
  • Coculture Techniques
  • Cytosine Deaminase / biosynthesis
  • Cytosine Deaminase / genetics
  • Cytosine Deaminase / metabolism
  • Flucytosine / pharmacokinetics
  • Flucytosine / pharmacology*
  • Genetic Therapy
  • Isoenzymes / genetics
  • Mice
  • Mice, Inbred C3H
  • Mice, Transgenic
  • Osteoclasts / drug effects
  • Osteoclasts / enzymology
  • Osteoclasts / pathology*
  • Osteoclasts / physiology
  • Promoter Regions, Genetic
  • Sarcoma / genetics
  • Sarcoma / metabolism
  • Sarcoma / pathology*
  • Sarcoma / therapy
  • Tartrate-Resistant Acid Phosphatase

Substances

  • Antimetabolites, Antineoplastic
  • Isoenzymes
  • Flucytosine
  • Acid Phosphatase
  • Acp5 protein, mouse
  • Tartrate-Resistant Acid Phosphatase
  • Cytosine Deaminase