The mammalian target of rapamycin complex 1 (mTORC1) is a master regulator of 
cell growth and proliferation. Recent studies have suggested that constitutive 
activation of mTORC1 in normal cells could lead to malignant tumor development 
in several tissues. However, the mechanisms of mTORC1 hyperactivation to promote 
the growth and metastasis of breast or other cancers are still not well 
characterized. Here, using a new inducible deletion system, we show that 
deletion of Tsc1 in mouse primary mammary tumor cells, either before or after 
their transplantation, significantly increased their growth in vivo. The 
increase in tumor growth was completely rescued by rapamycin treatment, 
suggesting a major contribution from mTORC1 hyperactivation. Interestingly, 
glucose starvation-induced autophagy, but not amino acid starvation-induced 
autophagy, was increased significantly in Tsc1-null tumor cells. Further 
analysis of these cells also showed an increased Akt activation but no 
significant changes in Erk signaling. Together, these results provide insights 
into the mechanism by which hyperactivation of mTORC1 promotes breast cancer 
progression through increasing autophagy and Akt activation in vivo.