Smad signal and TGFβ induced apoptosis in human lymphoma cells
Autor: | Judit Jánosi, László Kopper, Katalin Nagy, Lajos Berczi, Eszter Kohut, Sándor Paku, Gábor Barna, Rudolf Mihalik, Anna Sebestyén |
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Rok vydání: | 2005 |
Předmět: |
medicine.medical_specialty
Lymphoma Smad6 Protein Immunology Apoptosis Smad2 Protein SMAD Biology Biochemistry Peripheral blood mononuclear cell Smad7 Protein Transforming Growth Factor beta1 Transforming Growth Factor beta Cell Line Tumor hemic and lymphatic diseases Internal medicine medicine Humans Immunology and Allergy RNA Messenger Smad3 Protein B-cell lymphoma Molecular Biology Smad4 Protein Hematology medicine.disease BCL10 DNA-Binding Proteins Endocrinology Cell culture Trans-Activators Cancer research Signal Transduction Transforming growth factor |
Zdroj: | Cytokine. 30:228-235 |
ISSN: | 1043-4666 |
DOI: | 10.1016/j.cyto.2005.01.013 |
Popis: | Transforming growth factor beta1 (TGF beta1) has antiproliferative and/or apoptotic effect on lymphoid cells. In certain lymphomas exogenous TGF beta1 is able to induce apoptosis, however many lymphoid malignancies are resistant to the endogenous TGF beta1 production. We studied the expression and the activity of TGF beta1 signalling components in B cell lymphoma cell lines (e.g. HT 58 cells) and in isolated human peripheral mononuclear cells (PBMCs) from healthy individual's and B-CLL patient's blood. We found that all signal transducer Smads (Smad2,-3; Smad4) and at least one of the inhibitory Smads (Smad6,-7) were expressed in non-treated lymphoma cells, but the inhibitory Smads did not in normal/control PBMCs. However, after TGF beta1 treatment Smad6 disappeared, while the expression of Smad7 increased in HT 58 cells. The activity of Smad signals was proved by phosphorylation of Smad2, nuclear translocation of Smad2/3, and the increased expression of Smad-dependent gene, TIEG in TGF beta1 treated lymphoma cells. These results showed that Smad signaling is available in certain different human lymphoma cells, however ISmads expression could inhibit the signal transmission. This findings indicates that the lost sensitivity of lymphoma cells toward a physiological regulatory factor could be reversed. |
Databáze: | OpenAIRE |
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