Journal of Cancer Research and Clinical Oncology

, 137:1581

Introduction of pro-interleukin-16 inhibits T-lymphoblastic leukemia growth in mice

Authors

  • Jillian Richmond
    • Pulmonary CenterBoston University School of Medicine
  • Michael Finkel
    • Pulmonary CenterBoston University School of Medicine
  • Anna Studwell
    • Pulmonary CenterBoston University School of Medicine
  • Frederic Little
    • Pulmonary CenterBoston University School of Medicine
    • Pulmonary CenterBoston University School of Medicine
Rapid Communication

DOI: 10.1007/s00432-011-1017-x

Cite this article as:
Richmond, J., Finkel, M., Studwell, A. et al. J Cancer Res Clin Oncol (2011) 137: 1581. doi:10.1007/s00432-011-1017-x

Abstract

Purpose

Pro-interleukin-16 (pro-IL-16) is the precursor to mature interleukin-16 (IL-16) protein. Previous studies have demonstrated that pro-IL-16 can function as a regulator of cell cycle. A number of human T-cell leukemia and lymphoma cell lines are pro-IL-16 deficient. Intracellular expression of pro-IL-16 causes these cell lines to become quiescent, implicating loss of pro-IL-16 as a contributory step in T-cell malignancy. Therefore, we tested whether or not reintroduction of pro-IL-16 into solid tumors in mice could halt tumor growth.

Methods

MOLT-4 lymphoblastic leukemia cells were stably transfected with a dsRed-tomato virus and were injected subcutaneously into NOD/SCID/γ chain-knockout mice. Tumor growth was monitored with an in vivo imaging system. A pro-IL-16-GFP fusion virus or control GFP only virus was injected into the tumors, and mice were monitored for 1 week.

Results

Injection of the pro-IL-16-containing lentivirus inhibited growth of established MOLT-4 tumors in mice. Tumor explants exhibited diminished proliferative capacity.

Conclusions

Our data support the concept that restoration of pro-IL-16 expression in malignant T cells may have therapeutic value.

Keywords

Pro-interleukin-16Growth arrestMalignant T cellLymphoblastic leukemiaLentiviral vector

Copyright information

© Springer-Verlag 2011