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

doi:10.1016/j.bbrc.2016.07.099

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

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26 Scopus citations

Abstract

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 language	English (US)
Pages (from-to)	33-38
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	478
Issue number	1
DOIs	https://doi.org/10.1016/j.bbrc.2016.07.099
State	Published - Sep 9 2016

Keywords

Apoptosis
Ceramidase
Leukemia

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2016.07.099

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title = "ACER3 supports development of acute myeloid leukemia",

abstract = "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.",

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

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T1 - ACER3 supports development of acute myeloid leukemia

AU - Chen, Chen

AU - Yin, Yancun

AU - Li, Chunling

AU - Chen, Jinliang

AU - Xie, Jingjing

AU - Lu, Zhigang

AU - Li, Minjing

AU - Wang, Yuesi

AU - Zhang, Chengcheng

PY - 2016/9/9

Y1 - 2016/9/9

N2 - 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.

AB - 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.

KW - Apoptosis

KW - Ceramidase

KW - Leukemia

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ACER3 supports development of acute myeloid leukemia

Abstract

Keywords

ASJC Scopus subject areas

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