Bcl-2 expression and glucocorticoid-induced apoptosis of leukemic and lymphoma cells
| Autor: | van den Berg Jd, Smets La |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Cancer Research
CD3 Complex Lymphoma Apoptosis Biology Dexamethasone Mice Adenosine Triphosphate Proto-Oncogene Proteins medicine Tumor Cells Cultured Animals Humans Lymphocytes Glucocorticoids Leukemia Hematology medicine.disease Hedgehog signaling pathway BCL10 Cell biology Rats Gene Expression Regulation Neoplastic Oncology Lytic cycle Proto-Oncogene Proteins c-bcl-2 Homeostasis Glucocorticoid Cell Division medicine.drug |
| Zdroj: | Leukemialymphoma. 20(3-4) |
| ISSN: | 1042-8194 |
| Popis: | The lytic response of lymphoid cells to glucocorticoid hormones (GC) is prototypical of the induction of apoptosis: a special form of cellular demise for the removal of unwanted or redundant cells. Initiation and execution of a death programme are therefore major checkpoints in GC-sensitivity. Although Bcl-2 protein can prevent or delay apoptosis of lymphoma and leukemia cells, exposed to multiple cytotoxic agents, its antagonism of GC-induced apoptosis appears most critical in conferring resistance to corticosteroids. Moreover, Bcl-2 may modulate GC-signalling to apoptosis through its association with fundamental cellular processes such as energy state, Ca2+ homeostasis and transmembrane transport. However, this signalling pathway can also be interrupted by Bcl-2- independent mechanisms. This review discusses the various cellular and oncogenetic factors that control GC sensitivity of leukemia/lymphoma cells and proposes a hypothesis of how GC may induce a death programme, sensitive to blockade by Bcl-2. |
| Databáze: | OpenAIRE |
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