AI Article Synopsis
- Chordomas are rare tumors linked to the axial skeleton, and surgical removal is currently the best cure available.
- The study focused on the PI3K/mTOR pathway to determine if it was active in chordomas and if using the inhibitor PI-103 could reduce tumor growth and increase cell death.
- Results showed that the PI3K/mTOR pathway was active in chordomas, and treatment with PI-103 successfully reduced cell proliferation and increased apoptosis in the chordoma cell line UCH-1.
Article Abstract
Background: Chordomas are rare tumors of the axial skeleton for which surgical resection remains the most reliable means of cure. PI-103 is a inhibitor of PI3K/AKT and mTOR activation. This study aims to determine whether the PI3K/mTOR pathway was active in chordomas and whether their inhibition could lead to decreased proliferation and increased apoptosis.
Materials And Methods: Thirteen human chordoma were tested for activation of the PI3K/mTOR pathway. The human chordoma cell line UCH-1 was treated with increasing doses of PI-103. Inhibition of AKT and mTOR was examined and assays assessing proliferation and apoptosis were performed.
Results: The chordoma specimen demonstrated activation of the PI3K/mTOR pathway. PI-103 inhibited the AKT and mTOR activation in the UCH-1 cell line. PI-103 inhibited proliferation and induced apoptosis in UCH-1.
Conclusion: The PI3K/AKT and mTOR signaling pathway is constitutively activated in chordoma. PI-103 decreases proliferation and induces apoptosis in the UCH-1 via inhibition of the PI3K/mTOR pathway.
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