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Proposed mechanistic model. In untreated cancer, low TSC1/2 expression is associated with enhanced mTORC1 activity and, therefore, with a primary metastatic and stemness phenotype. In cancer treated for mTOR inhibition, EVI1-SOX9 become activated (in part by overexpression) and positively sustain the following features: mTOR signaling (through upregulation of RHEB and RAPTOR), metastatic potential (through LMS-up and other signatures) and stemness (through at least SOX9).
