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Tuberin-deficiency downregulates N-cadherin and upregulates vimentin in kidney tumor of TSC patients.

Liang S, Salas T, Gencaslan E, Li B, Habib SL - Oncotarget (2014)

Bottom Line: 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.Kidney tumors from TSC patients showed significant decrease in N-cadherin and significant increased in vimentin protein expression compared to control kidney tissues.

View Article: PubMed Central - PubMed

Affiliation: South Texas Veterans Health Care System, San Antonio, TX.

ABSTRACT
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.

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Proposed model of regulation of N-cadherin and vimentin in kidney angiomyolipomaDeficiency in tuberin upregulates vimentin and downregulates N-cadherin in kidney tumor of TSC patients. In addition, activation of Akt enhances vimnetin and decreases N-cadherin expression while activation of mTORC1/2 increases vimentin and decreases N-cadherin resulted in cell fibrosis progression in renal angiomyolipoma of tuberous sclerosis patients.
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Figure 7: Proposed model of regulation of N-cadherin and vimentin in kidney angiomyolipomaDeficiency in tuberin upregulates vimentin and downregulates N-cadherin in kidney tumor of TSC patients. In addition, activation of Akt enhances vimnetin and decreases N-cadherin expression while activation of mTORC1/2 increases vimentin and decreases N-cadherin resulted in cell fibrosis progression in renal angiomyolipoma of tuberous sclerosis patients.


Tuberin-deficiency downregulates N-cadherin and upregulates vimentin in kidney tumor of TSC patients.

Liang S, Salas T, Gencaslan E, Li B, Habib SL - Oncotarget (2014)

Proposed model of regulation of N-cadherin and vimentin in kidney angiomyolipomaDeficiency in tuberin upregulates vimentin and downregulates N-cadherin in kidney tumor of TSC patients. In addition, activation of Akt enhances vimnetin and decreases N-cadherin expression while activation of mTORC1/2 increases vimentin and decreases N-cadherin resulted in cell fibrosis progression in renal angiomyolipoma of tuberous sclerosis patients.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4196174&req=5

Figure 7: Proposed model of regulation of N-cadherin and vimentin in kidney angiomyolipomaDeficiency in tuberin upregulates vimentin and downregulates N-cadherin in kidney tumor of TSC patients. In addition, activation of Akt enhances vimnetin and decreases N-cadherin expression while activation of mTORC1/2 increases vimentin and decreases N-cadherin resulted in cell fibrosis progression in renal angiomyolipoma of tuberous sclerosis patients.
Bottom Line: 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.Kidney tumors from TSC patients showed significant decrease in N-cadherin and significant increased in vimentin protein expression compared to control kidney tissues.

View Article: PubMed Central - PubMed

Affiliation: South Texas Veterans Health Care System, San Antonio, TX.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus