Pharmacological inactivation of the PI3K p110δ prevents breast tumour progression by targeting cancer cells and macrophages.

ABSTRACT: Patient selection for PI3K-targeted solid cancer treatment was based on the PIK3CA/PTEN mutational status. However, it is increasingly clear that this is not a good predictor of the response of breast cancer cells to the anti-proliferative effect of PI3K inhibitors, indicating that isoform(s) other than p110α may modulate cancer cells sensitivity to PI3K inhibition. Surprisingly, we found that although no mutations in the p110δ subunit have been detected thus far in breast cancer, the expression of p110δ becomes gradually elevated during human breast cancer progression from grade I to grade III. Moreover, pharmacological inactivation of p110δ in mice abrogated the formation of tumours and the recruitment of macrophages to tumour sites and strongly affected the survival, proliferation and a

SUBMITTER: Goulielmaki E 

PROVIDER: S-EPMC5992183 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature