Today, despite current advances in combinatorial therapies such as surgery, radiotherapy and chemotherapy, aggressive cancers remain fatal. Cancer stem-like cells (CSCs) may account for chemotherapy resistance and thus represent a promising therapeutic target. In this context, the present inventors identified essential intracellular pathways favoring the self-renewal and survival of CSCs. More precisely, the present inventors showed that the cytokine co-receptor GP130 acts as a co-receptor for Apelin / APJ signaling and that the interaction of Apelin with APJ/GP130 activates a dual signaling pathway involving the Akt/mTOR and STAT3 transcription factor, thereby promoting CSCs survival and self-renewal. They therefore propose to block these pathways in order to treat patients suffering from tumors containing CSCs, such as glioblastomas.
