Acute myeloid leukemia cells induce senescence and adipogenic differentiation of mesenchymal stem cells in a tumor-supportive microenvironment at the same time.

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Acute myeloid leukemia (AML) actively induces the transformation of a normal hematopoietic niche into a tumor-supportive microenvironment. Among them, Mesenchymal stem cells (MSCs)are closely associated with the genesis and development of AML. MSCs derived from AML patients (AML-MSC) show a senescent state, with possibly biased differentiation ability. However, it remains unclear whether AML-MSC exhibits the dual pathological evolution of both senescence characteristics and lipogenic differentiation bias in the microenvironment at the same time. Thus, this study, by analyzing AML-MSC and MSC co-cultured with tumor cells over a long period， revealed that AML affects the AMPK/SIRT1 signaling pathway, inducing an increase in reactive oxygen species in the microenvironment of MSCs, thereby leading to significantly altered metabolic processes, adipose-biased differentiation capacity, and senescence of MSCs. These findings clarify the mechanism by which AML cells actively contribute to the evolution of the tumor microenvironment, providing a theoretical basis for future dual targeting of supportive ecological niches.

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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