Receptor-independent ectopic activity of PROLACTIN predicts aggressive lung tumors and indicates HDACi-based therapeutic strategies

ABSTRACT: Aim: PROLACTIN (PRL), normally produced by the pituitary gland, acts through its receptor (PRL-R) to initiate a signalling cascade to the genome. PRL can also be produced by cancer cells and become oncogenic by stimulating its receptor following an autocrine or paracrine route. Here we investigated the oncogenic activities of PRL in lung cancer. Results: PRL is ectopically activated in a subset of very aggressive lung tumours, associated with a rapid fatal outcome, in our cohort of 293 lung tumour patients as well as in an external independent series of patients. An investigation of the molecular basis of PRL adverse effects surprisingly showed an absence of PRL-R expression in the vast majority of PRL-expressing lung tumours. Additionally, a detailed analysis of the ectopically expressed

ORGANISM(S): Homo sapiens

SUBMITTER: Rousseaux Sophie 

PROVIDER: S-ECPF-GEOD-49544 | biostudies-other |

REPOSITORIES: biostudies-other