ERK-TSC2 signalling in constitutively-active HRAS mutant HNSCC cells promotes resistance to PI3K inhibition

Phosphoinositide 3-kinase (PI3K)/AKT/mTOR signalling regulates critical tumor cell functions, including cellular metabolism, survival, angiogenesis, growth and migration [1]. Hyper-activation of PI3K signalling is frequently observed in head and neck squamous cell carcinomas (HNSCCs), with nearly 80% of tumors containing amplifications or mutations of PIK3CA and numerous additional tumors containing losses of tumor suppressor PTEN or amplifications of EGFR or AKT1/2/3 [2 –4]. Owing to the prevalence of PI3K-pathway aberrations in HNSCC and the dependency of tumor cells on PI3K signalling for survival and growth, targeting this pathway is an attractive therapeutic strategy for HNSCC patients.
Source: Oral Oncology - Category: Cancer & Oncology Authors: Source Type: research