The Raf/MEK/ERK pathway can govern drug resistance, apoptosis and sensitivity to targeted therapy. (Articolo in rivista)

Type

• Articolo in rivista (Classe)
• Prodotto della ricerca (Classe)

Label

• The Raf/MEK/ERK pathway can govern drug resistance, apoptosis and sensitivity to targeted therapy. (Articolo in rivista) (literal)

Anno

• 2010-01-01T00:00:00+01:00 (literal)

Alternative label

• Abrams SL, Steelman LS, Shelton JG, Wong EW, Chappell WH, Bäsecke J, Stivala F, Donia M, Nicoletti F, Libra M, Martelli AM, McCubrey JA. (2010)
  The Raf/MEK/ERK pathway can govern drug resistance, apoptosis and sensitivity to targeted therapy.
  in Cell cycle (Georget. Tex.)
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Abrams SL, Steelman LS, Shelton JG, Wong EW, Chappell WH, Bäsecke J, Stivala F, Donia M, Nicoletti F, Libra M, Martelli AM, McCubrey JA. (literal)

Pagina inizio

• 1781 (literal)

Pagina fine

• 1791 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

• 9 (literal)

Rivista

• Cell cycle (Rivista)

Note

• ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• Department of Microbiology and Immunology; Brody School of Medicine at East Carolina University; Greenville, NC USA; Division of Hematology and Oncology; University of Göttingen; Göttingen, Germany; Department of Biomedical Sciences; University of Catania; Catania, Italy; Dipartimento di Scienze Anatomiche Umane e Fisiopatologia dell’Apparato Locomotore; Sezione di Anatomia Umana; Cell Signalling Laboratory; Università di Bologna; Bologna, Italy; (literal)

Titolo

• The Raf/MEK/ERK pathway can govern drug resistance, apoptosis and sensitivity to targeted therapy. (literal)

Abstract

• The effects of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR signaling pathways on proliferation, drug resistance, prevention of apoptosis and sensitivity to signal transduction inhibitors were examined in FL/DeltaAkt-1:ER*(Myr(+)) + DeltaRaf-1:AR cells which are conditionally-transformed to grow in response to Raf and Akt activation. Drug resistant cells were isolated from FL/DeltaAkt-1:ER*(Myr(+)) + DeltaRaf-1:AR cells in the presence of doxorubicin. Activation of Raf-1, in the drug resistant FL/DeltaAkt-1:ER*(Myr(+)) + DeltaRaf-1:AR cells, increased the IC(50) for doxorubicin 80-fold, whereas activation of Akt-1, by itself, had no effect on the doxorubicin IC(50). However, Akt-1 activation enhanced cell proliferation and clonogenicity in the presence of chemotherapeutic drugs. Thus the Raf/MEK/ERK pathway had profound effects on the sensitivity to chemotherapeutic drugs, and Akt-1 activation was required for the long term growth of these cells as well as resistance to chemotherapeutic drugs. The effects of doxorubicin on the induction of apoptosis in the drug resistant cells were enhanced by addition of either mTOR and MEK inhibitors. These results indicate that targeting the Raf/MEK/ERK and PI3K/Akt/mTOR pathways may be an effective approach for therapeutic intervention in drug resistant cancers that have mutations activating these cascades (literal)

Prodotto di

• Institute of molecular genetics (IGM) (Istituto)
• Bersagli molecolari per il controllo della progressione tumorale (ME.P03.012.001) (Modulo)

Autore CNR

• Alberto Maria Martelli (Persona)

Insieme di parole chiave

• Parole chiave di "The Raf/MEK/ERK pathway can govern drug resistance, apoptosis and sensitivity to targeted therapy." (Insieme di parole chiave)

Incoming links:

Prodotto

• Institute of molecular genetics (IGM) (Istituto)
• Bersagli molecolari per il controllo della progressione tumorale (ME.P03.012.001) (Modulo)

Autore CNR di

• Alberto Maria Martelli (Persona)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi

• Cell cycle (Rivista)

Insieme di parole chiave di

• Parole chiave di "The Raf/MEK/ERK pathway can govern drug resistance, apoptosis and sensitivity to targeted therapy." (Insieme di parole chiave)