Microarray and biochemical analysis of bufalin-induced apoptosis of HL-60 Cells.
Bufalin is a natural toxin with anti-leukemic properties. It induces cell differentiation and apoptosis, as well as increasing the sensitivity of leukemia cells to other chemotherapeutic agents. We investigated the biological effects and molecular mechanisms of bufalin triggered apoptosis in HL-60 cells by gene expression profiling. The broad transcriptional response to bufalin was consistent with bufalin's action of regulating HL-60 cell proliferation and apoptosis, as well as its synergistic effect with other drugs. Further transcription factor ELISA experiments suggested that the transcription factors NFkappaB and AP-1 were activated to promote bufalin-induced HL-60 cell apoptosis. Our study provides new insights into the molecular mechanisms of bufalin, might prove to be beneficial in leukemia therapy.
Chen
Ailiang
A
Medical Systems Biology Research Center, Tsinghua University School of Medicine, Beijing 100084, People's Republic of China.
Yu
Jian
J
Zhang
Liang
L
Sun
Yimin
Y
Zhang
Yan
Y
Guo
Hongyan
H
Zhou
Yuxiang
Y
Mitchelson
Keith
K
Cheng
Jing
J
D017209:Apoptosis; D002018:Bufanolides / Q000633:toxicity*; D049109:Cell Proliferation / Q000187:drug effects; D020869:Gene Expression Profiling; D018922:HL-60 Cells; D006801:Humans; D016328:NF-kappa B / Q000096:biosynthesis; D020411:Oligonucleotide Array Sequence Analysis; D018808:Transcription Factor AP-1 / Q000096:biosynthesis
D002018:Bufanolides; D016328:NF-kappa B; D018808:Transcription Factor AP-1; C022777:bufalin