Scorpion venom component III inhibits cell proliferation by modulating NF-κB activation in human leukemia cells.
Scorpion venom contains various groups of compounds that exhibit anticancer activity against a variety of malignancies through a poorly understood mechanism. While the aberrant activation of nuclear factor κB (NF-κB) has been linked with hematopoietic malignancies, we hypothesized that scorpion venom mediates its effects by modulating the NF-κB signaling pathway. In the present study, we examined the effects of scorpion venom component III (SVCIII) on the human leukemia cell lines THP-1 and Jurkat and focused on the NF-κB signaling pathway. Our results showed that SVCIII inhibited cell proliferation, caused cell cycle arrest at G1 phase and inhibited the expression of cell cycle regulatory protein cyclin D1 in a dose-dependent manner in THP-1 and Jurkat cells. SVCIII also suppressed the constitutive NF-κB activation through inhibition of the phosphorylation and degradation of IκBα. NF-κB luciferase reporter activity was also inhibited by SVCIII. Our data suggest that SVCIII, a natural compound, may exert its antiproliferative effects by inhibiting the activation of NF-κB and, thus, has potential use in the treatment of hematopoietic malignancies, alone or in combination with other agents.
Department of Pediatrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou; ; Department of Immunology, Xinxiang Medical University, Xinxiang;
Xiangfeng
X
Song
Guojun
G
Zhang
Aiping
A
Sun
Jiqiang
J
Guo
Zhongwei
Z
Tian
Hui
H
Wang
Yufeng
Y
Liu