Pérez-Ramírez Cristina, Cañadas-Garre Marisa, Molina Miguel Ángel, Faus-Dáder María José, Calleja-Hernández Miguel Ángel
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.
Department of Biochemistry. Faculty of Pharmacy. University of Granada Campus Universitario de Cartuja, s/n. 18071 Granada, Spain.
Pharmacogenomics. 2015 Nov;16(16):1843-62. doi: 10.2217/pgs.15.122. Epub 2015 Nov 10.
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.
非小细胞肺癌(NSCLC)是全球癌症死亡的主要原因。在过去几年中,激活型EGFR突变的发现使患者对酪氨酸激酶抑制剂的敏感性和疾病反应性增加,改变了NSCLC患者的治疗前景。PTEN/PI3K/AKT通路调节多种细胞功能,包括细胞生长、分化、增殖、存活、运动、侵袭和细胞内运输。该通路的改变,主要是PTEN失活,与NSCLC患者对EGFR酪氨酸激酶抑制剂治疗的耐药性及较低生存率相关。在本综述中,我们将简要讨论NSCLC中发现的主要PTEN/PI3K/AKT通路改变,以及PTEN/PI3K/AKT调节导致肿瘤发生的细胞过程。