Related Experiment Video
Updated: Apr 26, 2026

RhoC GTPase Activation Assay
Published on: August 22, 2010
mTOR regulate EMT through RhoA and Rac1 pathway in prostate cancer
XianGuo Chen1, HaiYan Cheng2,3, TengFei Pan1
1Department of Urology, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, PR China.
Abstract:
Recently, an increasing number of studies have suggested that mTOR plays a critical role in the regulation of tumor cell motility, invasion and cancer metastasis. However, little is known about the signaling mechanisms in regulating epithelial-mesenchymal transition (EMT) of prostate cancer. In this study, we found that the expression levels of Raptor and Rictor in prostate cancer tissues were elevated, which may suggest that Raptor and Rictor signaling pathways are associated with prostate cancer progression and metastasis. Inhibition of mTORC1 or mTORC2 by knock down of Raptor or Rictor, respectively, migration and invasion of prostate cancer were attenuated. Furthermore, EMT, a characterized by the changed expression levels of various markers like E-cadherin, β-catenin, N-cadherin, and vimentin emergend following inhibition of Raptor or Rictor. Finally, the small GTPases (RhoA and Rac1) which were crucial regulatory proteins in cell migration and invasion were inactivited after downregulating Raptor and Rictor. These results suggest that mTOR regulate EMT at least in part by down regulation of RhoA and Rac1 signaling pathways. Our findings provide novel very attractive target strategies that the inhibition of mTOR signaling pathways may retard prostate cancer migration and invasion at early stages.
Insights
mTOR signaling pathways, specifically Raptor and Rictor, are elevated in prostate cancer, driving tumor cell migration and invasion. Inhibiting these pathways can reduce metastasis by impacting epithelial-mesenchymal transition (EMT).
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Emerging research highlights the mechanistic target of rapamycin (mTOR) pathway's role in cancer cell motility, invasion, and metastasis.
- The specific signaling mechanisms by which mTOR regulates epithelial-mesenchymal transition (EMT) in prostate cancer remain largely unelucidated.
Purpose of the Study:
- To investigate the role of Raptor and Rictor, components of mTORC1 and mTORC2, in prostate cancer progression and metastasis.
- To elucidate the signaling pathways through which mTOR regulates EMT in prostate cancer cells.
Main Methods:
- Analysis of Raptor and Rictor expression levels in prostate cancer tissues.
- Inhibition of mTORC1 and mTORC2 via Raptor and Rictor knockdown.
- Assessment of prostate cancer cell migration and invasion.
- Evaluation of EMT markers (E-cadherin, β-catenin, N-cadherin, vimentin) and small GTPases (RhoA, Rac1) expression and activity.
Main Results:
- Elevated expression of Raptor and Rictor was observed in prostate cancer tissues, correlating with disease progression.
- Knockdown of Raptor or Rictor significantly attenuated prostate cancer cell migration and invasion.
- Inhibition of Raptor or Rictor led to changes in EMT markers and inactivation of RhoA and Rac1 signaling pathways.
Conclusions:
- mTOR signaling, through Raptor and Rictor, plays a critical role in regulating prostate cancer cell migration, invasion, and EMT.
- mTOR regulates EMT, at least partly, by downregulating RhoA and Rac1 signaling pathways.
- Inhibition of mTOR signaling pathways presents a promising therapeutic strategy to retard prostate cancer metastasis in early stages.
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
mTOR Signaling and Cancer Progression
PI3K/mTOR/AKT Signaling Pathway
Small GTPases - Ras and Rho
Three regulatory proteins control their activity:
MAPK Signaling Cascades
The Ras Gene
Ras is a...

