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Titolo:
Interactions between the PI3K and Raf signaling pathways can result in thetransformation of hematopoietic cells
Autore:
McCubrey, JA; Lee, JT; Steelman, LS; Blalock, WL; Moye, PW; Chang, FM; Pearce, M; Shelton, JG; White, MK; Franklin, RA; Pohnert, SC;
Indirizzi:
E Carolina Univ, Brody Sch Med, Dept Microbiol & Immunol, Greenville, NC 27858 USA E Carolina Univ Greenville NC USA 27858 Immunol, Greenville, NC 27858 USA E Carolina Univ, Brody Sch Med, Dept Biochem, Greenville, NC 27858 USA E Carolina Univ Greenville NC USA 27858 Biochem, Greenville, NC 27858 USA E Carolina Univ, Brody Sch Med, Leo Jenkins Canc Ctr, Greenville, NC 27858USA E Carolina Univ Greenville NC USA 27858 Canc Ctr, Greenville, NC 27858USA Thomas Jefferson Coll Med, Dept Pathol Anat & Cell Biol, Philadelphia, PA USA Thomas Jefferson Coll Med Philadelphia PA USA Biol, Philadelphia, PA USA
Titolo Testata:
CANCER DETECTION AND PREVENTION
fascicolo: 4, volume: 25, anno: 2001,
pagine: 375 - 393
SICI:
0361-090X(2001)25:4<375:IBTPAR>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASE; ABROGATE CYTOKINE DEPENDENCY; COLONY-STIMULATING FACTOR; GROWTH-FACTOR; AUTOCRINE TRANSFORMATION; GM-CSF; DIFFERENTIAL ABILITIES; BAD PHOSPHORYLATION; CELLULAR ONCOGENES; RETROVIRAL VECTORS;
Keywords:
PI3K; Akt; Raf; cytokines; hematopoietic cells; oncogenes; signal transduction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
69
Recensione:
Indirizzi per estratti:
Indirizzo: McCubrey, JA E Carolina Univ, Brody Sch Med, Dept Microbiol & Immunol, Brody Bldg 5N98C, Greenville, NC 27858 USA E Carolina Univ Brody Bldg 5N98C Greenville NC USA 27858 USA
Citazione:
J.A. McCubrey et al., "Interactions between the PI3K and Raf signaling pathways can result in thetransformation of hematopoietic cells", CANCER DET, 25(4), 2001, pp. 375-393

Abstract

The P13K/Akt and Raf/MEK/ERK signal transduction cascades are pivotal in transmitting signals from membrane receptors to downstream targets that regulate apoptosis, gene expression, and cell growth. The abilities of activated P13K, Akt, Raf, and MEK proteins to abrogate the cytokine dependence of three different hematopoietic cell lines were determined. Activated P13K or Akt expression by themselves did not efficiently annul cytokine dependence. Raf and MEK could abrogate the cytokine dependence of murine FDC-P1 and human TF-1 cells. however, the frequency of transformation was dependent on the particular oncogene examined, as more factor-independent cells were isolated after infection with activated retroviruses encoding A-Raf or Raf-1 than were with MEK1 or B-Raf. Cytokine-independent Delta Raf-1-infected cellsformed tumors on injection into immunocompromised mice, whereas cytokine-dependent cell lines did not, demonstrating the oncogenic effects of activation of the Raf/MEK/ERK pathway. Overexpression of the antiapoptotic Bcl-2 protein synergized with activation of the Raf/MEK/ERK cascade and increased the efficiency of transformation of FDC-P1 and TF-1 cells. In contrast to the results observed with FDC-P1 and TF-1 cells, the activated Raf genes didnot relieve the cytokine dependence of marine FL5.12 cells. The abilities of the Raf and P13K pathways to interact and annul the cytokine dependence of FL5.12 cells were determined. The combination of Raf and either P13K or Akt expression relieved cytokine dependence of some FL5.12 cells. and the efficiency of transformation could be enhanced further by Bcl-2 or Bcl-X-L overexpression. Thus, the antiapoptotic P13K/Akt and Bcl-2/Bcl-X-L proteins can interact with the growth-promoting Raf/MEK/ERK pathway and annul the cytokine dependence of certain hematopoietic cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 07:42:56