| First Author | Zhao X | Year | 2025 |
| Journal | Oncogene | Volume | 44 |
| Issue | 23 | Pages | 1820-1832 |
| PubMed ID | 40133477 | Mgi Jnum | J:365598 |
| Mgi Id | MGI:8187883 | Doi | 10.1038/s41388-025-03351-x |
| Citation | Zhao X, et al. (2025) Rictor orchestrates beta-catenin/FOXO balance by maintaining redox homeostasis during development of ovarian cancer. Oncogene |
| abstractText | Rictor/mTORC2 has been demonstrated to have important roles in cancer development and progression in a number of solid and hematologic malignancies. However, little is known about the role of Rictor/mTORC2 in ovarian cancer pathophysiology. Herein, using conditional Rictor knockout mice, we were able to demonstrate that Rictor deletion disrupted glutathione metabolism through AKT/Nrf2 signaling pathway and induced intracellular oxidative stress during the malignant transformation of Kras/Pten-mutant ovarian surface epithelial cells. Elevated reactive oxygen species and activated FOXO3a in Rictor-deleted cells strikingly shifts the functional interaction of beta-catenin from TCF to FOXO3a, which strongly inhibits classical Wnt/beta-catenin signaling. Our findings emphasize a pivotal role for Rictor in orchestrating crosstalk between the PI3K/AKT and Wnt/beta-catenin signaling in the development of ovarian cancer. Illustration of Rictor/mTORC2 in promoting tumor onset by regulating glutathione metabolism and mediating oncogenic signaling. |
