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Titolo:
Activation of c-Jun NH2-terminal kinase/stress-activated protein kinase (JNK/SAPK) is critical for hypoxia-induced apoptosis of human malignant melanoma
Autore:
Kunz, M; Ibrahim, S; Koczan, D; Thiesen, HJ; Kohler, HJ; Acker, T; Plate, KH; Ludwig, S; Rapp, UR; Brocker, EB; van Muijen, GNP; Flory, E; Gross, G;
Indirizzi:
Univ Rostock, Dept Dermatol & Venerol, D-18055 Rostock, Germany Univ Rostock Rostock Germany D-18055 & Venerol, D-18055 Rostock, Germany Univ Rostock, Inst Immunol, D-18055 Rostock, Germany Univ Rostock Rostock Germany D-18055 t Immunol, D-18055 Rostock, Germany Univ Erlangen Nurnberg, Dept Neuropathol, D-91054 Erlangen, Germany Univ Erlangen Nurnberg Erlangen Germany D-91054 -91054 Erlangen, Germany Univ Wurzburg, Inst Med Strahlenkunde & Zellforsch, D-97080 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97080 forsch, D-97080 Wurzburg, Germany Univ Wurzburg, Dept Dermatol, D-97080 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97080 rmatol, D-97080 Wurzburg, Germany Univ Nijmegen, Dept Pathol, NL-6500 Nijmegen, Netherlands Univ Nijmegen Nijmegen Netherlands NL-6500 NL-6500 Nijmegen, Netherlands Paul Ehrlich Inst, D-63225 Langen, Germany Paul Ehrlich Inst Langen Germany D-63225 h Inst, D-63225 Langen, Germany
Titolo Testata:
CELL GROWTH & DIFFERENTIATION
fascicolo: 3, volume: 12, anno: 2001,
pagine: 137 - 145
SICI:
1044-9523(200103)12:3<137:AOCNKP>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
STRESS-INDUCED APOPTOSIS; NF-KAPPA-B; INDUCED UP-REGULATION; CELL-DEATH; TRANSCRIPTION FACTORS; TNF RECEPTOR-1; SOLID TUMORS; EXPRESSION; PATHWAY; CERAMIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Kunz, M Univ Rostock, Dept Dermatol & Venerol, Augusten Str 80, D-18055 Rostock, Germany Univ Rostock Augusten Str 80 Rostock Germany D-18055 ock, Germany
Citazione:
M. Kunz et al., "Activation of c-Jun NH2-terminal kinase/stress-activated protein kinase (JNK/SAPK) is critical for hypoxia-induced apoptosis of human malignant melanoma", CELL GROWTH, 12(3), 2001, pp. 137-145

Abstract

Mitogen-activated protein kinase (MAPK) signaling was examined in malignant melanoma cells exposed to hypoxia, Here we demonstrate that hypoxia induced a strong activation of the c-Jun NH2-terminal kinase (JNK), also termed stress-activated protein kinase (SAPK), in the melanoma cell line 530 in vitro. Other members of the MAPK family, e.g,, extracellular signal-regulatedkinase and p38, remained unaffected by the hypoxic stimulus. Activated JNK/SAPK could also be observed in the vicinity of hypoxic tumor areas in melanoma metastases as detected by immunohistochemistry. Functional analysis ofJNK/SAPK activation in the melanoma cell line 530 revealed that activationof JNK/SAPK is involved in hypoxia-mediated tumor cell apoptosis, Both a dominant negative mutant of JNWSAPK (SAPK beta K -->R) and a dominant negative mutant of the immediate upstream activator of JNK/SAPK, SEK1 (SEK1 K -->R), inhibited hypoxia-induced apoptosis in transient transfection studies, In contrast, overexpression of the wild-type kinases had a slight proapoptotic effect. Inhibition of extracellular signal-regulated kinase and p38 pathways by the chemical inhibitors PD98058 and SB203580, respectively, had noeffect on hypoxia-induced apoptosis, Under normoxic conditions, no influence on apoptosis regulation was observed after inhibition of all three MAPK pathways. In contrast to recent findings, JNK/SAPK activation did not correlate with Fas or Fas ligand (FasL) expression, suggesting that the Fas/FasLsystem is not involved in hypoxia-induced apoptosis in melanoma cells. Taken together, our data demonstrate that hypoxia-induced JNK/SAPK activation appears to play a critical role in apoptosis regulation of melanoma cells in vitro and in vivo, independent of the Fas/FasL system.

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Documento generato il 22/09/20 alle ore 19:29:32