ArticleThe Prostate2020
Differential roles and activation of mammalian target of rapamycin complexes 1 and 2 during cell migration in prostate cancer cells.
Article in The Prostate, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Targeting RAC1 in glioblastoma: prognostic value, immune landscape, and small molecule therapeutic potential.Frontiers in oncology · 2026Article
- GαInternational journal of molecular sciences · 2025Article
- ALYREF recruits ELAVL1 to promote colorectal tumorigenesis via facilitating RNA m5C recognition and nuclear export.NPJ precision oncology · 2024Article
- Review
- Assessing the mechanism of fast-cycling cancer-associated mutations of Rac1 small Rho GTPase.Protein science : a publication of the Protein Society · 2024Article
- Rac1 promotes the reprogramming of glucose metabolism and the growth of colon cancer cells through upregulating SOX9.Cancer science · 2023Article
- Dual contribution of the mTOR pathway and of the metabolism of amino acids in prostate cancer.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Dual Inhibition of mTORC1/2 Reduces Migration of Cholangiocarcinoma Cells by Regulation of Matrixmetalloproteinases.Frontiers in cell and developmental biology · 2021Article
- Rac1, A Potential Target for Tumor Therapy.Frontiers in oncology · 2021Review
- Article
- Small Molecule Inhibitors Targeting GαCancers · 2020Article
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4 authors.
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Abstract
backgroundMammalian target of rapamycin (mTOR) is a downstream substrate activated by PI3K/AKT pathway and it is essential for cell migration. It exists as two complexes: mTORC1 and mTORC2. mTORC1 is known to be regulated by active AKT, but the activation of mTORC2 is poorly understood. In this study, we investigated the roles and differential activation of the two mTOR complexes during cell migration in prostate cancer cells.
methodsWe used small interfering RNA to silence the expression of Rac1 and the main components of mTOR complexes (regulatory associated protein of mTOR [RAPTOR] and rapamycin-insensitive companion of mTOR [RICTOR]) in LNCaP, DU145, and PC3 prostate cancer cell lines. We performed transwell migration assay to evaluate the migratory capability of the cells, and Western blot analysis to study the activation levels of mTOR complexes.
resultsSpecific knockdown of RAPTOR and RICTOR caused a decrease of cell migration, suggesting their essential role in prostate cancer cell movement. Furthermore, epidermal growth factor (EGF) treatments induced the activation of both the mTOR complexes. Lack of Rac1 activity in prostate cancer cells blocked EGF-induced activation of mTORC2, but had no effect on mTORC1 activation. Furthermore, the overexpression of constitutively active Rac1 resulted in significant increase in cell migration and activation of mTORC2 in PC3 cells, but had no effect on mTORC1 activation. Active Rac1 was localized in the plasma membrane and was found to be in a protein complex, with RICTOR, but not RAPTOR.
conclusionWe suggest that EGF-induced activation of Rac1 causes the activation of mTORC2 via RICTOR. This mechanism plays a critical role in prostate cancer cell migration.
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