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Activation of Nuclear Factor K B in Human Neuroblastoma Cell Lines
Author(s) -
Körner Marie,
Tarantino Nadine,
Pleskoff Olivier,
Lee Leo M.,
Debré Patrice
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.62051716.x
Subject(s) - cell culture , neuroblastoma , cellular differentiation , biology , phorbol , protein kinase c , microbiology and biotechnology , transcription factor , signal transduction , cytosol , sh sy5y , biochemistry , enzyme , genetics , gene
The nuclear factor K B (NF‐ k B) is a eukaryotic transcription factor. In B cells and macrophages it is constitutively present in cell nuclei, whereas in many other cell types, NF‐ K B translocates from cytosol to nucleus as a result of transduction by tumor necrosis factor α (TNFα), phorbol ester, and other polyclonal signals. Using neuro‐blastoma cell lines as models, we have shown that in neural cells NF‐ K B was present in the cytosol and translocated into nuclei as a result of TNFa treatment. The TNFα‐activated NF‐ K B was transcriptionally functional. NF‐ K B activation by TNFα was not correlated with cell differentiation or proliferation. However, reagents such as nerve growth factor (NGF) and the phorbol ester phorbol 12‐myristate 13‐acetate (PMA), which induce phenotypical differentiation of the SH‐SY5Y neuroblastoma cell line, activated NF‐ K B, but only in that particular cell line. In a NGF‐responsive rat pheochromocytoma cell line, PC12, PMA activated NF‐ K B, whereas NGF did not. In other neuroblastoma cell lines, such as SK‐N‐Be(2), the lack of PMA induction of differentiation was correlated with the lack of NF‐ k B activation. We found, moreover, that in SK‐N‐Be(2) cells protein kinase C (PKC) enzymatic activity was much lower compared with that in a control cell line and that the low PKC enzymatic activity was due to low PKC protein expression. NF‐ K B was not activated by retinoic acid, which induced morphological differentiation of all the neuroblastoma cell lines used in the present study. Thus, NF‐ K B activation was not required for neuroblastoma cell differentiation. Furthermore, the results obtained with TNFα proved that NF‐ K B activation was not sufficient for induction of neuroblastoma differentiation.