Brain-derived neurotrophic factor promotes survival and chemoprotection of human neuroblastoma cells
Autor: | Xiaoyan Zhu, David S. Middlemas, Junfang Zhou, Brenda K. Kihl |
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Rok vydání: | 1999 |
Předmět: |
medicine.medical_specialty
Neurite Cell Survival Cellular differentiation Antineoplastic Agents Tretinoin Tropomyosin receptor kinase B Biology Biochemistry Neuroblastoma Neurotrophic factors Internal medicine medicine Tumor Cells Cultured Humans Drug Interactions Phosphorylation Autocrine signalling Molecular Biology Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor Cell Differentiation Cell Biology Endocrinology Oncogene Proteins v-fos Phenotype nervous system Cell culture Cancer research Cisplatin Immediate early gene |
Zdroj: | The Journal of biological chemistry. 274(23) |
ISSN: | 0021-9258 |
Popis: | Brain-derived neurotrophic factor (BDNF) promotes neuronal survival and protection against neuronal damage. We addressed whether BDNF might promote survival and chemoprotection in neuroblastoma (NB) using a drug-sensitive human NB cell line. All-trans-retinoic acid (ATRA) induces a striking phenotypic differentiation of NB1643 cells, and exogenous BDNF treatment promotes survival of these differentiated cells. ATRA induces TRKB expression, and exogenous BDNF stimulates both autophosphorylation of TRKB and induction of the immediate early gene, FOS, in these cells. BDNF mRNA is expressed in NB1643 cells. Because the time course of TRKB induction closely parallels phenotypic differentiation of these cells, it seems probable that ATRA induces differentiation of NB1643 cells by establishing an autocrine loop involving BDNF and TRKB. Exogenous BDNF treatment resulted in a further increase in neurite outgrowth, which again suggests that an autocrine loop is involved in differentiation of NB1643 cells in response to ATRA. We then tested whether BDNF might afford drug resistance in NB and found that BDNF does indeed protect in this NB model against cisplatin, a DNA-damaging agent actually used in the treatment of NB. |
Databáze: | OpenAIRE |
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