Paclitaxel mediates the PI3K/AKT/mTOR pathway to reduce proliferation of FLT3 ‑ITD < sup > + < /sup > AML cells and promote apoptosis

Exp Ther Med. 2024 Feb 23;27(4):161. doi: 10.3892/etm.2024.12449. eCollection 2024 Apr.ABSTRACTAcute myeloid leukemia (AML) with internal tandem duplication (ITD) mutations in the FLT3 tyrosine kinase tend to have a poor prognosis. FLT3-ITD can promote the progress of AML by activating the PI3K/AKT/mTOR pathway. Paclitaxel (PTX) is a natural anticancer drug that has been widely used in chemotherapy for multiple malignancies. The present study used the CCK-8 assay, flow cytometry, PCR and western blotting to explore the anti-leukemia effect and possible mechanisms of PTX on MV4-11 cells with the FLT3-ITD mutation and the underlying mechanism. As a result, it was found that PTX could inhibit proliferation of MV4-11 cells and promoted apoptosis by inhibiting the PI3K/AKT/mTOR pathway.PMID:38476887 | PMC:PMC10928971 | DOI:10.3892/etm.2024.12449
Source: Experimental and Therapeutic Medicine - Category: General Medicine Authors: Source Type: research