PTEN and PI3K/AKT in non-small-cell lung cancer

Author:

Pérez-Ramírez Cristina12,Cañadas-Garre Marisa1,Molina Miguel Ángel3,Faus-Dáder María José2,Calleja-Hernández Miguel Ángel14

Affiliation:

1. Pharmacogenetics Unit. UGC Provincial de Farmacia de Granada. Instituto de Investigación Biosanitaria de Granada. Complejo Hospitalario Universitario de Granada. Avda. Fuerzas Armadas, 2. 18014 Granada, Spain

2. Department of Biochemistry. Faculty of Pharmacy. University of Granada Campus Universitario de Cartuja, s/n. 18071 Granada, Spain

3. PANGAEA BIOTECH, S.L. Hospital Universitario Quirón Dexeus. C/Sabino Arana, 5-19. 08028 Barcelona

4. Department of Pharmacology. Faculty of Pharmacy. University of Granada. Campus Universitario de Cartuja, s/n. 18071 Granada, Spain

Abstract

Non-small-cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide. In the last years, the identification of activating EGFR mutations, conferring increased sensitivity and disease response to tyrosine kinase inhibitors, has changed the prospect of NSCLC patients. The PTEN/PI3K/AKT pathway regulates multiple cellular functions, including cell growth, differentiation, proliferation, survival, motility, invasion and intracellular trafficking. Alterations in this pathway, mainly PTEN inactivation, have been associated with resistance to EGFR-tyrosine kinase inhibitor therapy and lower survival in NSCLC patients. In this review, we will briefly discuss the main PTEN/PI3K/AKT pathway alterations found in NSCLC, as well as the cell processes regulated by PTEN/PI3K/AKT leading to tumorigenesis.

Publisher

Future Medicine Ltd

Subject

Pharmacology,Genetics,Molecular Medicine

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