Abstract
The IL-2R signaling is critical for normal lymphocyte proliferation. However, the role of the IL-2 signaling in cervical cancer is not yet fully understood. We show that in IL-2R-expressing cervical cancer cells, JAK1 molecules are not phosphorylated. At low doses of IL-2, the constitutive phosphorylation of JAK3 and STAT5 increases in the tumor cells and decreases in lymphocytes, whereas the opposite occurs at high doses of IL-2. Using AG-490, the activation of JAK3 and the proliferation of cervical cancer cells were inhibited. We describe differences in the response of molecules downstream the IL-2R in lymphocytes and tumor cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents / pharmacology*
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Cell Line, Tumor
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Cell Proliferation / drug effects*
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Dose-Response Relationship, Drug
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Female
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Humans
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Interleukin-2 / pharmacology*
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Janus Kinase 1 / metabolism
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Janus Kinase 3 / metabolism*
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Lymphocytes / drug effects
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Lymphocytes / enzymology
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Lymphocytes / pathology
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Phosphorylation
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Receptors, Interleukin-2 / drug effects
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Receptors, Interleukin-2 / metabolism
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Recombinant Proteins / pharmacology
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STAT5 Transcription Factor / metabolism*
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Signal Transduction / drug effects
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Time Factors
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Uterine Cervical Neoplasms / enzymology*
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Uterine Cervical Neoplasms / pathology
Substances
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Antineoplastic Agents
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IL2 protein, human
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Interleukin-2
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Receptors, Interleukin-2
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Recombinant Proteins
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STAT5 Transcription Factor
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JAK1 protein, human
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JAK3 protein, human
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Janus Kinase 1
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Janus Kinase 3