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Titolo:
RAFTK/PYK2-dependent and -independent apoptosis in multiple myeloma cells
Autore:
Chauhan, D; Hideshima, T; Pandey, P; Treon, S; Teoh, G; Raje, N; Rosen, S; Krett, N; Husson, H; Avraham, S; Kharbanda, S; Anderson, KC;
Indirizzi:
Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA02115 USA Harvard Univ Boston MA USA 02115 t, Dept Adult Oncol, Boston, MA02115 USA Harvard Inst Med, Beth Israel Deaconess Med Ctr, Div Expt Med & Hematol Oncol, Boston, MA 02115 USA Harvard Inst Med Boston MA USA 02115 Hematol Oncol, Boston, MA 02115 USA Northwestern Univ, Sch Med, Robert H Lurie Canc Ctr, Chicago, IL 60611 USANorthwestern Univ Chicago IL USA 60611 ie Canc Ctr, Chicago, IL 60611 USA
Titolo Testata:
ONCOGENE
fascicolo: 48, volume: 18, anno: 1999,
pagine: 6733 - 6740
SICI:
0950-9232(19991118)18:48<6733:RA-AIM>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
FOCAL TYROSINE KINASE; HEMATOPOIETIC-CELLS; ACTIVATION; INTERLEUKIN-6; ASSOCIATION; PYK2; PHOSPHORYLATION; MEGAKARYOCYTES; STIMULATION; PAXILLIN;
Keywords:
multiple myeloma; irradiation; dexamethasone; apoptosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Anderson, KC Dana Farber Canc Inst, 44 Binney St, Boston, MA 02215 USA Dana Farber Canc Inst 44 Binney St Boston MA USA 02215 15 USA
Citazione:
D. Chauhan et al., "RAFTK/PYK2-dependent and -independent apoptosis in multiple myeloma cells", ONCOGENE, 18(48), 1999, pp. 6733-6740

Abstract

Related Adhesion Focal Tyrosine Kinase (RAFTK; also known as Pyk2), is a member of the Focal Adhesion Kinase (FAK) subfamily and is activated by TNF alpha, UV light and increases in intracellular calcium levels. However, thefunction of RAFTK remains largely unknown. Our previous studies demonstrated that treatment with dexamethasone (Dex), ionizing radiation (IR), and anti-Fas mAb induces apoptosis in multiple myeloma (MM) cells. In the presentstudy, we examined the potential role of RAFTK during induction of apoptosis in human MM cells triggered by these three stimuli. Dex-induced apoptosis, in contrast to apoptosis triggered by anti-Fas mAb or IR, is associated with activation of RAFTK. Transient overexpression of RAFTK wild type (RAFTK WT) induces apoptosis, whereas transient overexpression of Kinase inactive RAFTK (RAFTK K-M) blocks Dex-induced apoptosis. In contrast, transient overexpression of RAFTK K-M has no effect on apoptosis triggered by IR or Fas. In Dex-resistant cells, Dex does not trigger either RAFTK activation or apoptosis. Finally, interleukin-6 (IL-6), a known survival factor for MM cells, inhibits both activation of RAFTK and apoptosis of MM.1S cells triggered by Dex. Our studies therefore demonstrate Dex-induced RAFTK-dependent, and IR or Fas induced RAFTK-independent apoptotic signaling cascades in MM cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 07:46:28