When mTORC2-AKT signaling meets cell polarity

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Daulat, Avais M. | Borg, Jean-Paul

Edité par CCSD ; Taylor & Francis -

International audience. Hyperactivation of the mTOR-AKT pathway frequently contributes to the spread of cancer cells, especially in aggressive breast cancer, to distant organs, promoting the lethal metastatic program. Despite advances in the understanding of this signaling pathway and the development of inhibitors, efforts are still needed to dissect its complexity. This is particularly the case for mTORC2, which constitutes one of the two major branches of the mTOR pathway and whose mode of regulation is poorly defined. The mTORC2 complex consists of RICTOR, an evolutionarily conserved protein associated to mTOR, LST8 and SIN1, which is responsible for the phosphorylation of AGC protein kinases (AKT, SGK1 and PKCα). In a recent report1, we reveal that, in breast cancer cells, the mTORC2 complex, through the RICTOR subunit, can associate with PRICKLE1, a core member of planar cell polarity (PCP) which normally shapes organs during embryogenesis of Metazoans (Figure 1).

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