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J Cancer Res Clin Oncol. 2011 Oct;137(10):1581-5. doi: 10.1007/s00432-011-1017-x. Epub 2011 Aug 5.

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

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1
Pulmonary Center, Boston University School of Medicine, Boston, MA 02118, USA.

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.

PMID:
21818556
DOI:
10.1007/s00432-011-1017-x
[Indexed for MEDLINE]
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