Related Experiment Video
Updated: Aug 11, 2025

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
Published on: June 6, 2025
LAPTM4B promotes AML progression through regulating RPS9/STAT3 axis
Yongxiu Huang1, Meixi Peng2, Huanhuan Qin3
1School of Medicine, Chongqing University, Chongqing 400044, China; Department of Hematology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing 400038, China.
Abstract:
Acute myeloid leukemia (AML) is a heterogeneous disorder with high morbidity and mortality under the existing treatment strategy. Here, we found that lysosome-associated protein transmembrane 4 beta (LAPTM4B) was frequently upregulated in AML, and high LAPTM4B was associated with poor outcome. Moreover, LAPTM4B promoted leukemia progression in vitro and in vivo. Mechanically, LAPTM4B interacted with RPS9, and positively regulated RPS9 protein stability, which enhanced leukemia cell progression via activating STAT3. Our findings indicate for the first time that LAPTM4B contributes to leukemia progression in a RPS9/STAT3-dependent manner, suggesting that LAPTM4B may serve as a promising target for treatment of AML.
Insights
Lysosome-associated protein transmembrane 4 beta (LAPTM4B) is upregulated in acute myeloid leukemia (AML), promoting disease progression. Targeting LAPTM4B may offer a new therapeutic strategy for AML patients.
Area of Science:
- Oncology
- Molecular Biology
- Hematology
Background:
- Acute myeloid leukemia (AML) presents a significant clinical challenge due to its heterogeneity and poor outcomes with current treatments.
- Lysosome-associated protein transmembrane 4 beta (LAPTM4B) has been observed to be frequently upregulated in AML.
- High LAPTM4B expression correlates with adverse prognostic indicators in AML patients.
Purpose of the Study:
- To investigate the role of LAPTM4B in the progression of acute myeloid leukemia.
- To elucidate the molecular mechanisms underlying LAPTM4B-mediated leukemia progression.
- To evaluate LAPTM4B as a potential therapeutic target for AML.
Main Methods:
- Analysis of LAPTM4B expression levels in AML patient samples.
- In vitro and in vivo experiments to assess the functional impact of LAPTM4B on leukemia.
- Co-immunoprecipitation assays to identify interacting proteins.
- Western blotting and gene silencing techniques to study protein interactions and signaling pathways.
Main Results:
- LAPTM4B was frequently upregulated in AML and associated with poor patient outcomes.
- Overexpression of LAPTM4B enhanced leukemia cell proliferation and progression both in vitro and in vivo.
- LAPTM4B was found to interact with RPS9, stabilizing its protein levels.
- The LAPTM4B/RPS9 interaction led to the activation of STAT3, promoting leukemia progression.
Conclusions:
- LAPTM4B plays a critical role in promoting acute myeloid leukemia progression through a RPS9/STAT3-dependent pathway.
- LAPTM4B represents a novel and promising therapeutic target for AML treatment.
- Understanding the LAPTM4B/RPS9/STAT3 axis offers new insights into AML pathogenesis.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Abnormal Proliferation
The JAK-STAT Signaling Pathway
MAPK Signaling Cascades

