ACER3 supports development of acute myeloid leukemia

Chen Chen, Yancun Yin, Chunling Li, Jinliang Chen, Jingjing Xie, Zhigang Lu, Minjing Li, Yuesi Wang, Chengcheng Zhang

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


No new therapy for acute myeloid leukemia (AML) has been approved for more than 30 years. To effectively treat AML, new molecular targets and therapeutic approaches must be identified. In silico analysis of several databases of AML patients demonstrated that the expression of alkaline ceramidase 3 (ACER3) significantly inversely correlates with the overall survival of AML patients. To determine whether ACER3 supports AML development, we employed an shRNA-encoding lentivirus system to inhibit acer3 expression in human AML cells including NB4, U937, and THP-1 cells. The ACER3 deficiency resulted in decreased cell growth and colony formation, elevated apoptosis, and lower AKT signaling of leukemia cells. Our study indicates that ACER3 contributes to AML pathogenesis, and suggests that alkaline ceramidase inhibition is an option to treat AML.

Original languageEnglish (US)
Pages (from-to)33-38
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number1
StatePublished - Sep 9 2016


  • Apoptosis
  • Ceramidase
  • Leukemia

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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