Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Induction of cytosolic phospholipase A(2) by oncogenic Ras is mediated through the JNK and ERK pathways in rat epithelial cells
Autore:
Van Putten, V; Refaat, Z; Dessev, C; Blaine, S; Wick, M; Butterfield, L; Han, SY; Heasley, LE; Nemenoff, RA;
Indirizzi:
Univ Colorado, Hlth Sci Ctr, Div Renal Dis & Hypertens, Dept Med, Denver, CO 80262 USA Univ Colorado Denver CO USA 80262 pertens, Dept Med, Denver, CO 80262 USA Univ Colorado, Hlth Sci Ctr, Dept Pharmacol, Denver, CO 80262 USA Univ Colorado Denver CO USA 80262 r, Dept Pharmacol, Denver, CO 80262 USA
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 2, volume: 276, anno: 2001,
pagine: 1226 - 1232
SICI:
0021-9258(20010112)276:2<1226:IOCPAB>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
SIGNAL-TRANSDUCTION PATHWAYS; SYNTHASE-2 GENE-EXPRESSION; PROTEIN-KINASE PATHWAY; SMOOTH-MUSCLE CELLS; LUNG-CANCER CELLS; C-JUN; GROWTH-FACTOR; TRANSCRIPTION FACTOR; CYTOKINE GENES; ALPHA-ACTIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Nemenoff, RA Univ Colorado, Hlth Sci Ctr, Div Renal Dis & Hypertens, Dept Med, 4200 E 9th Ave,Box C-281, Denver, CO 80262 USA Univ Colorado 4200 E 9th Ave,Box C-281 Denver CO USA 80262 SA
Citazione:
V. Van Putten et al., "Induction of cytosolic phospholipase A(2) by oncogenic Ras is mediated through the JNK and ERK pathways in rat epithelial cells", J BIOL CHEM, 276(2), 2001, pp. 1226-1232

Abstract

Mutations in ras genes have been detected with high frequency in nonsmall cell lung cancer cells (NSCLC) and contribute to transformed growth of these cells. It has previously been shown that expression of oncogenic forms ofRas in these cells is associated with elevated expression of cytosolic phospholipase A(2) (cPLA(2)) and cyclooxygenase-2 (COX-2), resulting in high constitutive levels of prostaglandin production. To determine whether expression of constitutively active Res is sufficient to induce expression of these enzymes in nontransformed cells, normal lung epithelial cells were transfected with H-Ras, Stable expression of H-Ras increased expression of cPLA(2) and COX-2 protein. Transient transfection with II-Pas increased promoteractivity for both enzymes. H-Ras expression also activated all three families of MAP kinase: ERKs, JNKs, and p38 MAP kinase, Expression of constitutively active Raf did not increase either cPLA(2) or COX-2 promoter activity,but inhibition of the ERK pathway with pharmacological agents or expression of dominant negative ERK partially blocked the H-Ras-mediated induction of cPLA(2) promoter activity. Expression of dominant negative JNK kinases decreased cPLA(2) promoter activity in NSCLC cell lines and inhibited H-Ras-mediated induction in normal epithelial cells, whereas expression of constructs encoding constitutively active JNKs increased promoter activity. Inhibition of p38 MAP kinase or NF-KB had no effect on cPLA(2) expression. Truncational analysis revealed that the region of the cPLA(2) promoter from -58 to +12 contained sufficient elements to mediate H-Ras induction. We concludethat expression of oncogenic forms of Res directly increases cPLA(2) expression in normal epithelial cells through activation of the JNK and ERR pathways.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 23:02:49