# Vitexin Attenuates the Growth and Glycolysis of Acute Myeloid Leukemia Cells by Suppressing the HIF‐1α‐Modulated YAP Pathway Under Hypoxic Conditions

## TL;DR

Vitexin reduces the growth and energy production of leukemia cells under low oxygen by targeting a specific molecular pathway.

## Contribution

This study reveals a novel mechanism by which vitexin inhibits hypoxia-induced AML cell growth through the HIF-1α/YAP pathway.

## Key findings

- Vitexin inhibits hypoxia-induced AML cell viability and proliferation.
- Vitexin suppresses glycolytic markers like glucose uptake and lactate production.
- Vitexin blocks HIF-1α and YAP activation under hypoxia.

## Abstract

Vitexin, an apigenin flavone glycoside, exhibits antitumor activity against various cancers including leukemia. Hypoxia enhances glycolysis, thereby promoting tumor growth. In this study, we aimed to explore the effects of vitexin on hypoxia‐induced growth and glycolysis in acute myeloid leukemia (AML) cells and determine the underlying molecular mechanisms. Our findings showed that vitexin inhibited the hypoxia‐induced increase in viability and proliferation of AML cells. Vitexin suppressed glucose uptake, lactate production, and the expression of hexokinase 2, pyruvate kinase M2, and lactate dehydrogenase A in hypoxia‐exposed AML cells. Vitexin also blocked the hypoxia‐induced increase in hypoxia‐inducible factor 1α (HIF‐1α) and Yes‐associated protein (YAP) expression, as well as the decrease in p‐YAP expression. In addition, our results demonstrate that the YAP pathway is regulated by HIF‐1α in hypoxia‐exposed AML cells and participates in the inhibitory effects of vitexin on hypoxia‐induced AML cell growth and glycolysis. These results indicate that vitexin prevents hypoxia‐induced growth and glycolysis in AML cells by regulating the HIF‐1α/YAP signaling pathway.