The rictor phosohorylation is growth factor dependent in the breast cancer cells

Abstract

In spite of advances in early diagnosis breast cancer remains a dreadful disease,
approximately 40,000 women die every year. Deregulation of growth factor signaling has been
assigned as a hallmark in cancer development and progression. A multi-step process driven by a
highly selective pressure takes place in transformation of mammary epithelial cells and development
of malignant phenotype. Activation of cellular signaling pathways engaged in regulation of cell
proliferation, survival, and migration is a key factor in tumorigenesis. In this regard, one of the
most frequently activated signaling component in human cancer is Akt that provides leverage for
cancer cells in up-regulation of cellular proliferation and survival required for sustained tumor growth.
In our previous work we have identified mammalian Target of Rapamycin Complex 2 (mTORC2)
as a crucial regulator of Akt. An important role of the novel mTORC2 complex as a regulator
of Akt attracts a great interest in cancer research. The central hypothesis of this study is that
during cellular transformation the mTORC2 signaling is up-regulated to activate the Akt pathway
as an important step in development of primary breast cancer tumors. According our study, the
development of the novel breast cancer marker based on indirect evaluation of the mTORC2 activity
is feasible. Besides, it will be highly valuable to develop a specific inhibitor of mTORC2 to target
the breast cancer linked to hyperactivation of Akt. The study of mTORC2 regulation is a promising
area of research for development the breast cancer therapeutics. The novel breast cancer marker
will identify the mTORC2-dependent types of breast cancers and be applied for early diagnostics
and characterization of breast cancer. Development of a specific inhibitor of mTORC2 will provide
the specific targeting tool to suppress the growth factor signaling in breast cancer.