Study on Apoptosis of Human Promyelocytic Leukemia HL-60 Cells Induced by Fucosterol via Death Receptor Pathway

Abstract:

The purpose of this study is to investigate the effect of fucosterol on the induction of apoptosis and the molecular mechanism involved in Human promyelocytic leukemia HL-60 Cells. HL-60 Cells were treated with different concentrations of fucosterol at different time. MTT method was used to study fucosterol anti-tumor activity. Morphology observation was performed to determine the effects of fucosterol on apoptosis of HL-60 cells. Flow cytometry (FCM) was used to detect the cell cycle. Laser scanning confocal microscope (LSCM) was used to analyze the expressions of Fas, FasL, Fadd and Caspase-8. Caspase activity kits were used to determine the activity of Caspase-8 and Caspase-3. The results showed fucosterol could inhibit the growth of HL-60 cells, and the apoptosis morphology for 48 h treatment was obvious, which showed cell protuberance, cytoplasm concentrated and apoptotic body. Fucosterol treatment for 24 h increased the protein expression of Fas, FasL, Fadd and Caspase-8. It also showed that the activity of Caspase-3 and Caspase-8 has increased significantly. In conclusion, Fucosterol could induce HL-60 cells apoptosis via death receptor pathway.

• Periodical: Advanced Materials Research (Volume 790)
• Pages: 607-610
• DOI: https://doi.org/10.4028/www.scientific.net/AMR.790.607
• Online since: September 2013
• Authors: Yu Bin Ji, Dong Xue Song, Chen Feng Ji
• Keywords: Apoptosis, Death Receptor Pathway, Fucosterol, Human Promyelocytic Leukemia

References

[1] Yoo MS, Shin JS, Choi HE, et al. Fucosterol isolated from Undaria pinnatifida inhibits lipo-polysaccharide-induced production of nitric oxide and pro-inflammatory cytokines via the inactivation of nuclear factor-κB and p.38 mitogen-activated protein kinase in RAW264. 7 macrophages. Food Chem. Vol. 135 (2012).

DOI: 10.1016/j.foodchem.2012.05.039

[2] Khanavi M, Gheidarloo R, Sadati N, et al. Cytotoxicity of fucosterol containing fraction of marine algae against breast and colon carcinoma cell line. Pharmacogn Mag. Vol. 8 (2012), p.60.

DOI: 10.4103/0973-1296.93327

[3] Villa-Morales M, Fernández-Piqueras J. Targeting the Fas/FasL signaling pathway in cancer therapy. Expert Opin Ther Targets. Vol. 16 (2012), p.85.

DOI: 10.1517/14728222.2011.628937

[4] Lavrik IN, Krammer PH. Regulation of CD95/Fas signaling at the DISC. Cell Death Differ. Vol. 19 (2012), p.36.

DOI: 10.1038/cdd.2011.155

[5] Gordon N, Kleinerman ES. Aerosol therapy for the treatment of osteosarcoma lung metastases: targeting the Fas/FasL pathway and rationale for the use of gemcitabine. J Aerosol Med Pulm Drug Deliv. Vol. 23 (2010), p.189.

DOI: 10.1089/jamp.2009.0812

[6] Robert A, Newman Yang, Alison PY, et al. Cardiac glycosides as novel cancer therapeutic agents. Mol. Interv. Vol. 8 (2008), p.36.

[7] Zhao Y, Sui X, Ren H. From procaspase-8 to caspase-8: revisiting structural functions of caspase-8. J Cell Physiol. Vol. 225 (2010), p.316.

DOI: 10.1002/jcp.22276

[8] Galluzzi L, Kepp O, Kroemer G. Caspase-3 and prostaglandins signal for tumor regrowth in cancer therapy. Oncogene. Vol. 31 (2012), p.2805.

DOI: 10.1038/onc.2011.459