We investigated the role of mTORC2 signaling on the acquired docetaxel -resistant PC-3 cells to identify potential methods for clinical treatment. MTORC2 expression is essential for docetaxel drug resistance of PC-3 cells. The mTORC1/2 inhibitor AZD8055 caused more significant disruption of mTORC2 kinase activity than the mTORC1 inhibitor Rapamycin, which lead to decreased docetaxel-mediated resistance. Therefore, reversing docetaxel resistance, may become a therapeutic option in the treatment of mCRPC patients.
Keyphrases
- locally advanced
- end stage renal disease
- ejection fraction
- chronic kidney disease
- newly diagnosed
- poor prognosis
- squamous cell carcinoma
- cell proliferation
- prognostic factors
- tyrosine kinase
- mass spectrometry
- risk assessment
- rectal cancer
- binding protein
- combination therapy
- protein kinase
- climate change
- patient reported