Macrocalyxin A inhibits proliferation and induces apoptosis of t (8;21) leukemia cells through mitochondrial signaling pathways and regulates AML‑ETO mRNA expression

Wang,Zhenni; Lv,Yaping; Xia,Jun; Shi,Hao; Wang,Weizhong; Zhou,Yonglie

doi:10.3892/mmr.2015.3855

Macrocalyxin A inhibits proliferation and induces apoptosis of t (8;21) leukemia cells through mitochondrial signaling pathways and regulates AML‑ETO mRNA expression

Authors:
- Zhenni Wang
- Yaping Lv
- Jun Xia
- Hao Shi
- Weizhong Wang
- Yonglie Zhou
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Affiliations: Clinical Laboratory Center, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China, College of Pharmacy, Zhejiang University of Technology, Hangzhou, Zhejiang 310014, P.R. China
Published online on: May 27, 2015 https://doi.org/10.3892/mmr.2015.3855
Pages: 3537-3542

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Abstract

Progress in the last decade has improved the treatment of acute myeloid leukemia (AML); however, the treatment of AML is also demanding and better treatments are required. The present study aimed to examine the antiproliferative and proapoptotic effects of macrocalyxin A (MA), a novel deterpenid compound, on AML cells. It was identified that MA significantly inhibits kasumi‑1 cell proliferation in a time‑ and dose‑dependent manner. Furthermore, low concentrations of MA were able to induce kasumi‑1 cell differentiation; however, high concentrations of MA induced kasumi‑1 cell apoptosis. MA was also able to increase the expression of mitochondrial membrane protein in a dose‑dependent manner while the ∆Ψm was reduced. Additionally, Bad expression in kasumi‑1 cells was increased when treated with MA, indicating that the intrinsic apoptotic pathway may be important in MA‑induced kasumi‑1 cell apoptosis, where the mitochondrial permeability transition pore is opened and the ΔΨm is reduced. In addition, it was demonstrated that AML‑ETO mRNA may also be important in MA‑induced apoptosis.

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