Related Experiment Video
Updated: Sep 11, 2025

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
Published on: June 6, 2025
Alpha-enolase promotes progression of acute myeloid leukemia via MAPK/ERK signaling pathway
Shanshan Zhang1,2, Haina Wang1,3, Xuehong Zhang4
1Department of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, the Second Hospital of Dalian Medical University, Dalian 116027, China.
Abstract:
Due to the limited availability of effective treatment therapies, patients with refractory and relapsed acute myeloid leukemia (AML) often have poor prognoses. Therefore, identifying new therapeutic targets to improve the treatment landscape and enhance AML outcomes is critical. In this study, we demonstrated for the first time that alpha-enolase (ENO1) is markedly overexpressed in AML and is closely associated with poor prognosis. In vitro experiments revealed that ENO1 knockdown (shENO1) significantly inhibited cell proliferation and invasion, and concomitantly induced cell cycle arrest. In vivo, a mouse model engrafted with U937-shENO1 cells exhibited markedly prolonged overall survival compared with a model implanted with U937 cells. Mechanistically, ENO1 operates by activating the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway, as evidenced by the reversal of shENO1 function through ERK activation. Collectively, our findings highlight ENO1 as a promising therapeutic target in AML.
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