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Transfection of TRK-A into human neuroblastoma cells restores their ability to differentiate in response to nerve growth factor
Department of Pathology, University of Uppsala, University Hospital, Uppsala, Sweden.
Department of Pathology, University of Uppsala, University Hospital, Uppsala, Sweden.
Department of Pathology, University of Uppsala, University Hospital, Uppsala, Sweden.
Department of Pathology, University of Uppsala, University Hospital, Uppsala, Sweden.ORCID iD: 0000-0001-8889-5803
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1995 (English)In: Cell growth & differentiation, ISSN 1044-9523, Vol. 6, p. 727-736Article in journal (Refereed) Published
Abstract [en]

Human neuroblastoma cell lines frequently express the TRK-A proto-oncogene and bind nerve growth factor (NGF) but do not differentiate when exposed to NGF. Transient transfection of an exogenous TRK-A gene into SH-SY5Y and LA-N-5 neuroblastoma cells restored the ability of these tumor cells to differentiate with NGF. Stable TRK-A-transfected SH-SY5Y cell clones were isolated, and they responded to NGF by autophosphorylation of p140trk-A, c-fos induction, morphological differentiation, and increased expression of two neuronal marker genes, neuropeptide tyrosine and GAP-43. In phorbol ester-induced differentiated wild-type cells, TRK-A expression was increased with no change in NGF responsiveness. Thus, the restoration of the NGF-induced differentiation pathway by exogenous TRK-A presents a system of NGF-responsive human cultured cells and focuses attention on the trk-A protein and its function or malfunction in neuroblastoma.

Place, publisher, year, edition, pages
American Association of Cancer Research , 1995. Vol. 6, p. 727-736
National Category
Medical and Health Sciences Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:oru:diva-79035ISI: A1995RC82800013PubMedID: 7669728Scopus ID: 2-s2.0-0029042738OAI: oai:DiVA.org:oru-79035DiVA, id: diva2:1386327
Funder
Swedish Childhood Cancer FoundationSwedish Cancer SocietyMagnus Bergvall Foundation
Note

This work was supported by The Swedish Cancer Society, The Children Cancer Foundation of Sweden, HKH Kronprinsessan Lovisas Förening för Barnasjukvård, Hans von Kantzows, and Ollie och Elof Ericssons Stiftelser (to S.P.), and The Swedish Natural Science Research Council and Magnus Bergvalls Stiftelse (to E.N.).

Available from: 2013-10-20 Created: 2020-01-17 Last updated: 2020-01-28Bibliographically approved

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