Journal of Blood Disorders & Transfusion

AKT2 and CCAAT/enhancer-binding protein β transcription factor (C/EBP- β) mediate SphK1 up-regulation in imanitib-resistant K562 cells

3^rd International Conference on Hematology & Blood Disorders

November 02-04, 2015 Atlanta, USA

Gabriella Marfe1, Giovanna Mirone2, Carla Di Stefano3, Stefania Perna1 and Arvind Shukla4

1Second University of Naples, Italy 2Regina Elena National Cancer Institute, Italy 3Tor Vergata University, Italy 4Dr. D.Y. Patil University, India

Posters-Accepted Abstracts: J Blood Disord Transfus

Abstract:

In our previous study, we have shown that SphK1 is up-regulated in imatinib-resistant CML cells by a pathway contingent on a phosphoinositide 3-kinase/AKT2/mammalian target of rapamycin signaling pathway. In order to better understand this mechanism, we examined the signaling pathways responsible for transcriptional up-regulation of SphK1in imatinib-resistant CML cells. Pharmacological and molecular approaches demonstrated that only activation of AKT2, in addition to the CCAAT/enhancerbinding protein-β transcription factor is involved in transcriptional up-regulation of SphK1 in imanitib-resistance CML cells. Our data implicate AKT2 as an important mediator signaling in imanitib resistance leading to up-regulation of SphK1 and point to SphK1 and sphingosine-1-phosphate production as potential therapeutic targets in CML

Biography :

Email: gabriellamarfe@libero.it gabmarfe@alice.it