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

Acute 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.