Angiomyolipomas (AMLs) are associated with cell
fibrosis in kidney of
Tuberous Sclerosis Complex patients. The mechanism by which the fibrotic
proteins accumulated in AMLs has not been explored. In the present study, we investigated the role of Akt/
tuberin/mTOR pathway in the regulation cell
fibrosis proteins. AML cells that expressed low levels of
tuberin showed less expression of
N-cadherin and higher of
vimentin proteins compared to HEK293 cells. AML cells infected with Ad-
tuberin showed a significant decrease in
vimentin and an increase in
N-cadherin protein expression. In addition, cells treated with
rapamycin showed a significant increase in p-Akt and a decrease in p-p70S6K that was associated with a decrease expression of
vimentin and a slight increase expression in
N-cadherin. On the other hand, cells treated with Akt inhibitor revealed a significant decrease in p-Akt and p-p70S6K that was associated with a significant decrease in
vimentin and an increase in
N-cadherin expression. In addition, cells transfected with DN-Akt or DN-S6K show significant increase expression in
N-cadherin and a decrease in
vimentin. Moreover, cells transfected with
siRNA against rictor or
siRNA against raptor resulted in a decrease in
vimentin and an increase
N-cadherin expression. Kidney
tumors from
TSC patients showed significant decrease in
N-cadherin and significant increased in
vimentin protein expression compared to control kidney tissues. These data comprise the first report to provide the role of Akt/
tuberin/
mTORC1/2 in the regulation of
N-cadherin and
vimentin that are involved in the progression of
fibrosis in kidney
tumor of
TSC patients.