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Updated: Mar 21, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
Published on: June 6, 2025
Alisertib induces apoptosis and autophagy through targeting the AKT/mTOR/AMPK/p38 pathway in leukemic cells
Yunfeng Fu1, Yanan Zhang1, Meng Gao1
1The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China.
Abstract:
Alisertib, a potent and selective Aurora kinase A inhibitor, has been demonstrated to exert potent anti-cancer effects in pre-clinical and clinical studies. However, mechanisms of action of alisertib, including the molecular pathways involved in alisertib-induced apoptosis and autophagy of leukemic cells, have remained elusive. The aim of the present study was to investigate the effects of alisertib on cell growth, apoptosis and autophagy and to delineate the possible molecular mechanisms in leukemic cells. Acid phosphatase, MTT and Annexin V/propidium iodide staining assays as well as immunostaining for light chain 3B showed that treatment of the REH leukemia cell line with alisertib exerted potent growth inhibitory effects, and induced apoptosis and autophagy in a dose‑dependent manner. Western blot analysis indicated that these effects may be attributed to the suppression of the activity of the Akt/mammalian target of rapamycin/5'-AMP-dependent kinase/p38 mitogen-activated protein kinase signaling pathways in REH cells. The present study confirmed that alisertib may represent a promising autophagy-inducing drug for the treatment of leukemia and shed light on its molecular mechanism of action.
Insights
Alisertib, an Aurora kinase A inhibitor, effectively inhibits leukemia cell growth, inducing apoptosis and autophagy. This study reveals its mechanism involves suppressing key signaling pathways, highlighting alisertib as a potential leukemia treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Alisertib is a potent Aurora kinase A inhibitor with demonstrated anti-cancer effects.
- The precise molecular mechanisms underlying alisertib's effects on leukemia, particularly apoptosis and autophagy, remain unclear.
Purpose of the Study:
- To investigate the impact of alisertib on leukemia cell growth, apoptosis, and autophagy.
- To elucidate the molecular pathways involved in alisertib-induced cell death and autophagy in leukemia cells.
Main Methods:
- Utilized acid phosphatase, MTT, and Annexin V/propidium iodide assays for cell viability and apoptosis.
- Employed immunostaining for light chain 3B and Western blot analysis to assess autophagy and signaling pathway activity.
Main Results:
- Alisertib significantly inhibited REH leukemia cell line growth in a dose-dependent manner.
- Alisertib treatment induced both apoptosis and autophagy in leukemia cells.
- Western blot analysis indicated suppression of Akt/mTOR/AMPK/p38 MAPK signaling pathways.
Conclusions:
- Alisertib exhibits potent anti-leukemic effects by inducing apoptosis and autophagy.
- The mechanism involves the suppression of critical signaling pathways, including Akt/mTOR/AMPK/p38 MAPK.
- Alisertib shows promise as an autophagy-inducing therapeutic agent for leukemia treatment.
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