Abstract
Glucocorticoids (GCs) cause apoptosis and cell cycle arrest in lymphoid cells and are used in the therapy of lymphoid malignancies. SLA (Src-like-adaptor), an inhibitor of T- and B-cell receptor signaling, is a promising candidate derived from expression profiling analyses in children with acute lymphoblastic leukemia (ALL). Over-expression and knock-down experiments in ALL in vitro model revealed that transgenic SLA alone had no effect on survival or cell cycle progression, nor did it affect sensitivity to, or kinetics of, GC-induced apoptosis. Although SLA is a prominent GC response gene, it does not seem to contribute to the anti-leukemic effects of GC.
Copyright (c) 2009 Elsevier Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing / antagonists & inhibitors
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Adaptor Proteins, Signal Transducing / genetics*
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Adaptor Proteins, Signal Transducing / metabolism
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Adaptor Proteins, Signal Transducing / physiology*
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Antineoplastic Agents / therapeutic use
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Cells, Cultured
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Doxycycline / pharmacology
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Doxycycline / therapeutic use
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Drug Resistance, Neoplasm / genetics
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Gene Expression Regulation, Leukemic / drug effects*
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Glucocorticoids / pharmacology*
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Glucocorticoids / therapeutic use
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Humans
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Jurkat Cells
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Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics*
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Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
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Proto-Oncogene Proteins pp60(c-src) / antagonists & inhibitors
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Proto-Oncogene Proteins pp60(c-src) / genetics*
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Proto-Oncogene Proteins pp60(c-src) / metabolism
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Proto-Oncogene Proteins pp60(c-src) / physiology*
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RNA, Small Interfering / pharmacology
Substances
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Adaptor Proteins, Signal Transducing
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Antineoplastic Agents
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Glucocorticoids
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RNA, Small Interfering
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SLA protein, human
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Proto-Oncogene Proteins pp60(c-src)
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Doxycycline