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[Cancer Research 63, 642-646, February 1, 2003]
© 2003 American Association for Cancer Research

Immunology

Non-Small Cell Lung Cancer-derived Soluble Mediators Enhance Apoptosis in Activated T Lymphocytes through an I{kappa}B Kinase-dependent Mechanism1

Raj K. Batra2, Ying Lin2, Sherven Sharma, Mariam Dohadwala, Jie Luo, Mehis Pold and Steven M. Dubinett3

Department of Medicine and The Lung Cancer Research Program [R. K. B., Y. L., S. S., M. D., J. L., M. P., S. M. D.], Jonsson Comprehensive Cancer Center [R. K. B., S. M. D.], University of California at Los Angeles and Veterans Administration-Greater Los Angeles Health Care System, Los Angeles, California 90095

T lymphocyte survival is critical for the development and maintenance of an effective host antitumor immune response; however, the tumor environment can negatively impact T-cell survival. Lymphocytes exposed to tumor supernatants (TSNs) were evaluated for apoptosis after mitogen stimulation. TSN was observed to significantly enhance phorbol 12-myristate 13-acetate/ionomycin- and anti-CD3-stimulated lymphocyte apoptosis. Enhanced lymphocyte apoptosis was associated with an impairment of nuclear factor {kappa}B nuclear translocation and diminished I{kappa}B{alpha} degradation. In lymphocytes stimulated after exposure to TSNs, cytoplasmic I{kappa}B{alpha} persisted as a result of alterations in I{kappa}B kinase (IKK) activity. Accordingly, although there were no apparent differences in IKK component concentrations, lymphocytes preexposed to TSNs exhibited markedly reduced IKK activity. We conclude that non-small cell lung cancer-derived soluble factors promote apoptosis in activated lymphocytes by an IKK-dependent pathway.




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Copyright © 2003 by the American Association for Cancer Research.