The
mammalian target of rapamycin (mTOR) acts in two structurally and functionally distinct
protein complexes, mTOR complex 1 (
mTORC1) and mTOR complex 2 (
mTORC2). Upon deregulation, activated mTOR signaling is associated with multiple processes involved in
tumor growth and
metastasis. Compared with
mTORC1, much less is known about
mTORC2 in
cancer, mainly because of the unavailability of a selective inhibitor. However, existing data suggest that
mTORC2 with its two distinct subunits Rictor and mSin1 might play a more important role than assumed so far. It is one of the key effectors of the PI3K/AKT/mTOR pathway and stimulates cell growth, cell survival, metabolism, and cytoskeletal organization. It is not only implicated in
tumor progression,
metastasis, and the tumor microenvironment but also in resistance to
therapy. Rictor, the central subunit of
mTORC2, was found to be upregulated in different kinds of
cancers and is associated with advanced
tumor stages and a bad prognosis. Moreover, AKT, the main downstream regulator of
mTORC2/Rictor, is one of the most highly activated
proteins in
cancer. Primary and secondary
liver cancer are major problems for current
cancer therapy due to the lack of specific medical treatment, emphasizing the need for further therapeutic options. This review, therefore, summarizes the role of
mTORC2/Rictor in
cancer, with special focus on primary
liver cancer but also on liver
metastases.