system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: AMP-Activated Protein Kinases, Antineoplastic Agents, Cell Line, Tumor, Cyclin D1, Cyclin-Dependent Kinase Inhibitor p21, Dose-Response Relationship, Drug, Esophageal Neoplasms, Humans, Metformin, Protein Stability, RNA, Small Interfering, Ribosomal Protein S6 Kinases, 70-kDa, Signal Transduction, TOR Serine-Threonine Kinases, Tumor Suppressor Protein p53, Ubiquitin Thiolesterase, Ubiquitin-Specific Peptidase 7, Up-Regulation.
user
Does metformin inhibit esophagus cancer proliferation through upregulation of USP7? Context: Recent population studies suggest that the use of metformin is associated with reduced incidence and improved prognosis of certain cancers. In the current study, we assessed the effect of metformin on esophagus cancer cells using two cell lines (Eca-109 and TE-1 cells). We found that metformin inhibited growth and decreased expression of cell-cycle regulators in these cells. Treatment with metformin was also associated with activation of AMP kinase and inhibition of mTOR/p70S6K/pS6 signaling in both cells. However, inhibition of AMPK signaling has little impact on the anti-proliferative roles of metformin. In addition, we found USP7, a positive regulator of tumor suppressor p53, as a new molecular target of metformin. Esophagus cancer cells can be protected against metformin-induced growth inhibition by small interfering RNA against USP7.
assistant
These results provide evidence for a mechanism that may contribute to the antineoplastic effects of metformin suggested by recent population studies and justify further work to explore potential roles for it in esophagus cancer prevention and treatment. Final Decision: yes