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Titolo:
Induction of oocyte maturation by jun-N-terminal kinase (JNK) on the oncogenic ras-p21 pathway is dependent on the raf-MEK signal transduction pathway
Autore:
Chie, L; Amar, S; Kung, HF; Lin, MCM; Chen, H; Chung, DL; Adler, V; Ronai, Z; Friedman, FK; Robinson, RC; Kovac, C; Brandt-Rauf, PW; Yamaizumi, Z; Michl, J; Pincus, MR;
Indirizzi:
Vet Adm Med Ctr, Dept Pathol & Lab Med, Brooklyn, NY 11209 USA Vet Adm MedCtr Brooklyn NY USA 11209 l & Lab Med, Brooklyn, NY 11209 USA Long Isl Univ, Dept Biol, Brooklyn, NY 11201 USA Long Isl Univ Brooklyn NY USA 11201 iv, Dept Biol, Brooklyn, NY 11201 USA Long Isl Univ, Dept Chem, Brooklyn, NY 11201 USA Long Isl Univ Brooklyn NY USA 11201 iv, Dept Chem, Brooklyn, NY 11201 USA NCI, Lab Biochem Physiol, Frederick, MD 21702 USA NCI Frederick MD USA 21702 , Lab Biochem Physiol, Frederick, MD 21702 USA CUNY, Mt Sinai Med Ctr, Ruttenberg Canc Ctr, New York, NY 10029 USA CUNY New York NY USA 10029 r, Ruttenberg Canc Ctr, New York, NY 10029 USA NCI, Mol Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA NCI Bethesda MD USA 20892 Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA Columbia Univ, Sch Publ Hlth, Div Environm Hlth Sci, New York, NY 10032 USA Columbia Univ New York NY USA 10032 ronm Hlth Sci, New York, NY 10032 USA NCI, Tokyo, Japan NCI Tokyo JapanNCI, Tokyo, Japan SUNY Hlth Sci Ctr, Dept Pathol, Brooklyn, NY 11203 USA SUNY Hlth Sci Ctr Brooklyn NY USA 11203 pt Pathol, Brooklyn, NY 11203 USA Dept Microbiol, Brooklyn, NY USA Dept Microbiol Brooklyn NY USADept Microbiol, Brooklyn, NY USA Dept Anat & Cell Biol, Brooklyn, NY USA Dept Anat & Cell Biol Brooklyn NYUSA Anat & Cell Biol, Brooklyn, NY USA
Titolo Testata:
CANCER CHEMOTHERAPY AND PHARMACOLOGY
fascicolo: 6, volume: 45, anno: 2000,
pagine: 441 - 449
SICI:
0344-5704(200006)45:6<441:IOOMBJ>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASES; MOLECULAR-DYNAMICS; BINDING DOMAIN; XENOPUS OOCYTES; RAF-P74 PROTEIN; P21 PROTEIN; MAP KINASE; WILD-TYPE; INHIBITION; COMPLEXES;
Keywords:
oncogenic ras-p21; oocyte maturation; dominant negative mutant of raf;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Pincus, MR Vet Adm Med Ctr, Dept Pathol & Lab Med, 800 Poly Pl, Brooklyn, NY 11209 USA Vet Adm Med Ctr 800 Poly Pl Brooklyn NY USA 11209 NY 11209 USA
Citazione:
L. Chie et al., "Induction of oocyte maturation by jun-N-terminal kinase (JNK) on the oncogenic ras-p21 pathway is dependent on the raf-MEK signal transduction pathway", CANC CHEMOT, 45(6), 2000, pp. 441-449

Abstract

Purpose: We have previously found that microinjection of activated MEK (mitogen activated kinase kinase) and ERK (mitogen-activated protein; MAP kinase) fails to induce oocyte maturation, but that maturation, induced by oncogenic ras-p21 and insulin-activated cell ras-p21, is blocked by peptides from the ras-binding domain of raf. We also found that jun kinase (JNK), on the stress-activated protein (SAP) pathway, which is critical to the oncogenic ras-p21 signal transduction pathway, is a strong inducer of oocyte maturation. Our purpose in this study was to determine the role of the raf-MEK-MAP kinase pathway in oocyte maturation and how it interacts with JNK from the SAP pathway. Methods: We microinjected raf dominant negative mutant mRNA(DN-raf) and the MEK-specific phosphatase, MKP-T4, either together with oncogenic p21 or c-raf mRNA, into oocytes or into oocytes incubated with insulin to determine the effects of these raf-MEK-MAP kinase pathway inhibitors. Results: We found that oocyte maturation induced by both oncogenic and activated normal p21 is inhibited by both DN-raf and by MKP-T4. The latter more strongly blocks the oncogenic pathway. Also an mRNA encoding a constitutively activated MEK strongly induces oocyte maturation that is not inhibited by DN-raf or by MKP-T4. Surprisingly, we found that oocyte maturation induced by JNK is blocked both by DN-raf and MKP-T4. Furthermore, we discovered that c-raf induces oocyte maturation that is inhibited by glutathione-S-transferase (GST), which we have found to be a potent and selective inhibitor of JNK. Conclusion: We conclude that there is a strong reciprocal interaction between the SAP pathway involving JNK and the raf-MEK-MAP kinase pathway and that oncogenic ras-p21 can be preferentially inhibited by MEK inhibitors. The results imply that blockade of both MEK and JNK-oncogenic ras-p21interactions may constitute selective synergistic combination chemotherapyagainst oncogenic ras-induced tumors.

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Documento generato il 20/01/20 alle ore 10:16:40