Neurotrophins and Trk Receptors in Primitive Neuroectodermal Tumor Cell Lines

Neurotrophins and Trk Receptors in Primitive Neuroectodermal Tumor Cell Lines AbstractOBJECTIVE:Primitive neuroectodermal tumors (PNETs) are thought to be derived from early central nervous system precursors. Therefore, we hypothesized that the neurotrophins (nerve growth factor, brain-derived neurotrophic factor, and neurotrophin-3) and their receptors (TrkA, TrkB, and TrkC), which are involved in the proliferation, differentiation, and survival of neuronal cells, might be important in regulating tumor growth.METHODS:Using ribonucleic acid (RNA) blotting and reverse transcription-polymerase chain reaction analysis, we investigated the expression of these ligands and their receptors in six PNET cell lines (Daoy, PFSK, D283 Med, UW288-1, CHP707m, and D341 Med). Neurotrophin protein levels were measured using enzyme- linked immunosorbent assay procedures. Receptor function was demonstrated by autophosphorylation. Induction of c-Fos expression and effects on cell proliferation were assessed after the addition of exogenous neurotrophin.RESULTS:Three cell lines expressed messenger RNA for all neurotrophins, whereas the other three expressed two of the three neurotrophins. Neurotrophin protein levels were low. All cell lines expressed messenger RNA. Five expressed the amino terminus of trkB, but three of these did not express the carboxyl terminus. All cell lines contained trkC messenger RNA, but the receptor was truncated in two cell lines. No cell line contained message for a receptor containing an insertion in the tyrosine kinase domain. The addition of neurotrophin to PNET cells resulted in phosphorylation of a protein that was immunoprecipitated with an anti-pan-Trk antibody. c-Fos expression and cell growth were increased by preincubation with neurotrophins, but only in the cell lines expressing the relevant full-length receptors.CONCLUSION:The expression of neurotrophins and neurotrophin receptors by PNET cell lines is variable. The presence of activated Trk receptors in these cell lines may be required for rapid growth, via an autocrine loop mechanism. This will require further investigation. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurosurgery Oxford University Press

Neurotrophins and Trk Receptors in Primitive Neuroectodermal Tumor Cell Lines

Neurotrophins and Trk Receptors in Primitive Neuroectodermal Tumor Cell Lines

Neurotrophins and Trk Receptors in Primitive Neuroectodermal Tumor Cell Lines Sharon A. Chiappa, D.Phil., Lawrence S. Chin, M.D., Russell H. Zurawel, Ph.D., Corey Raffel, M.D., Ph.D. D e p a r t m e n t o f N e u r o - O n c o l o g y ( S A C , R H Z , C R ) , M a y o C l i n i c a n d F o u n d a t i o n , R o c h e s t e r , M i n n e s o t a , a n d D e p a r t m e n t o f N e u r o l o g i c a l S u r g e r y ( L S C ) , U n i v e r s i t y o f M a r y l a n d , B a l t i m o r e , M a r y l a n d O BJEC T IV E: Prim itive neuroectodermal tumors (PNETs) are thought to be derived from early central nervous system precursors. Therefore, we hypothesized that the neurotrophins (nerve growth factor, brain-derived neurotrophic factor, and neurotrophin-3) and their receptors (TrkA, TrkB, and TrkC), which are involved in the proliferation, differentiation, and survival of neuronal cells, might be important in regulating tumor growth. M E T H O D S : Using ribonucleic acid (R N A ) blotting and reverse transcription-polym erase chain reaction analysis, we investigated the expression of these ligands and their receptors in six PN ET cell lines (D aoy, PFSK, D283 M ed, UW288-1, CHP707m , and D341 M ed). N eurotrophin protein levels w ere measured using enzyme- linked immunosorbent assay procedures. Receptor function was dem onstrated by autophosphorylation. Induction of c-Fos expression and effects on cell proliferation w ere assessed after the addition of exogenous neurotrophin. RESULTS: Three cell lines expressed messenger RNA for all neurotrophins, whereas the other three expressed two of the three neurotrophins. Neurotrophin protein levels were low. All cell lines expressed messenger RNA. Five expressed the amino terminus of t r k B , but three of these did not express the carboxyl terminus. All cell lines contained t r k C messenger RNA, but the receptor was truncated in two cell lines. No cell line contained message for a receptor containing an insertion in the...
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Publisher
Congress of Neurological Surgeons
Copyright
© Published by Oxford University Press.
ISSN
0148-396X
eISSN
1524-4040
D.O.I.
10.1097/00006123-199911000-00026
Publisher site
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Abstract

AbstractOBJECTIVE:Primitive neuroectodermal tumors (PNETs) are thought to be derived from early central nervous system precursors. Therefore, we hypothesized that the neurotrophins (nerve growth factor, brain-derived neurotrophic factor, and neurotrophin-3) and their receptors (TrkA, TrkB, and TrkC), which are involved in the proliferation, differentiation, and survival of neuronal cells, might be important in regulating tumor growth.METHODS:Using ribonucleic acid (RNA) blotting and reverse transcription-polymerase chain reaction analysis, we investigated the expression of these ligands and their receptors in six PNET cell lines (Daoy, PFSK, D283 Med, UW288-1, CHP707m, and D341 Med). Neurotrophin protein levels were measured using enzyme- linked immunosorbent assay procedures. Receptor function was demonstrated by autophosphorylation. Induction of c-Fos expression and effects on cell proliferation were assessed after the addition of exogenous neurotrophin.RESULTS:Three cell lines expressed messenger RNA for all neurotrophins, whereas the other three expressed two of the three neurotrophins. Neurotrophin protein levels were low. All cell lines expressed messenger RNA. Five expressed the amino terminus of trkB, but three of these did not express the carboxyl terminus. All cell lines contained trkC messenger RNA, but the receptor was truncated in two cell lines. No cell line contained message for a receptor containing an insertion in the tyrosine kinase domain. The addition of neurotrophin to PNET cells resulted in phosphorylation of a protein that was immunoprecipitated with an anti-pan-Trk antibody. c-Fos expression and cell growth were increased by preincubation with neurotrophins, but only in the cell lines expressing the relevant full-length receptors.CONCLUSION:The expression of neurotrophins and neurotrophin receptors by PNET cell lines is variable. The presence of activated Trk receptors in these cell lines may be required for rapid growth, via an autocrine loop mechanism. This will require further investigation.

Journal

NeurosurgeryOxford University Press

Published: Nov 1, 1999

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