Upregulation of EMP3 in acute myeloid leukemia: a study based on data mining, RT-qPCR and immunohistochemistry

Angui Liu1, Cong Yu2, Xianwei Peng1

  • 1Department of Hematology, The Second Affiliated Hospital of Guangxi Medical University, No.166, Daxue Road, Nanning, 530000, Guangxi Zhuang Autonomous Region, People's Republic of China.

Discover Oncology
|September 1, 2025
PubMed
Abstract

Insights

Epithelial Membrane Protein 3 (EMP3) is overexpressed in acute myeloid leukemia (AML), and its levels are linked to patient prognosis. Further research is needed to understand its role in AML development.

Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Epithelial Membrane Protein 3 (EMP3) is implicated in various cancers.
  • Its role in acute myeloid leukemia (AML) is not well understood.

Purpose of the Study:

  • To investigate EMP3 expression patterns in AML.
  • To determine the clinical significance and prognostic value of EMP3 in AML.
  • To explore the molecular mechanisms underlying EMP3's function in AML.

Main Methods:

  • Analysis of public datasets for EMP3 mRNA expression in AML patients and healthy donors.
  • Validation of EMP3 expression using reverse transcription quantitative PCR (RT-qPCR) and immunohistochemistry.
  • Prognostic evaluation through survival analysis.
  • Investigation of molecular mechanisms via weighted gene co-expression network analysis (WGCNA), single-cell RNA sequencing, and pathway enrichment analysis.

Main Results:

  • EMP3 mRNA and protein expression were significantly elevated in AML samples compared to healthy controls.
  • Higher EMP3 levels were associated with poorer clinical outcomes in AML patients.
  • Pathway enrichment analysis identified AML-related pathways and key co-expressed genes (BCL2A1, ITGAM) linked to EMP3.

Conclusions:

  • EMP3 is overexpressed in acute myeloid leukemia.
  • EMP3 expression levels may serve as a prognostic biomarker in AML.
  • EMP3 potentially plays a role in AML pathogenesis and progression.

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