Melanoma is the one of the most aggressive and less curable cancer, and
yet the molecular mechanisms of the aggressiveness remains elusive.
Melanoma cells resist to oxidative stress with hyperactive S6 ribosomal
protein which is important for protein synthesis. We hypothesize that
melanoma cells are resistant to oxidative stress due to constitutive
activation of AKT/mTOR pathway, leading to the aggressive phenotype. To
test the hypothesis, we set out four specific aims. (1) To investigate
the expression of other family members of EGFR, including HerbB2, 3, and
4. (2) To investigate the role of mTORC1 and mTORC2 in S6 activation.
(3) To investigate the crosstalk between MEK/ERK and PI3K/AKT/mTOR
pathway. (4) To investigate whether mTORC1 is required for melanoma
cells to sustain elevated oxidative stress. We will train students by
involving students in all stages of the project.