Biology:HL60
The HL-60 cell line is a human leukemia cell line that has been used for laboratory research on blood cell formation and physiology. HL-60 proliferates continuously in suspension culture in nutrient and antibiotic chemicals. The doubling time is about 36–48 hours. The cell line was derived from a 36-year-old woman who was originally reported to have acute promyelocytic leukemia at the MD Anderson Cancer Center.[1] HL-60 cells predominantly show neutrophilic promyelocytic morphology.[1] Subsequent evaluation, including the karyotype that showed absence of the defining t(15;17) translocation, concluded that HL-60 cells are from a case of AML FAB-M2 (now referred to as AML with maturation (WHO)).[2] Proliferation of HL-60 cells occurs through the transferrin and insulin receptors, which are expressed on cell surface. The requirement for insulin and transferrin is absolute, as HL-60 proliferation immediately ceases if either of these compounds is removed from the serum-free culture media.[3] With this line, differentiation to mature granulocytes can be induced by compounds such as dimethyl sulfoxide (DMSO), or retinoic acid. Other compounds like 1,25-dihydroxyvitamin D3, 12-O-tetradecanoylphorbol-13-acetate (TPA) and GM-CSF can induce HL-60 to differentiate to monocytic, macrophage-like and eosinophil phenotypes, respectively.
The HL-60 cultured cell line provides a continuous source of human cells for studying the molecular events of myeloid differentiation and the effects of physiologic, pharmacologic, and virologic elements on this process. HL-60 cell model was used to study the effect of DNA topoisomerase (topo) IIα and IIβ on differentiation and apoptosis of cells[4] and is especially useful in dielectrophoresis studies,[5] which require an aqueous environment with suspended and round cells. Furthermore, these cells have been used in order to investigate whether intracellular calcium plays a role in caspase activation induced by reactive oxygen species.[6]
Chromatin and gene expression profiling in HL-60 cells and differentiated cells derived from these has been performed recently.[7]
References
- ↑ 1.0 1.1 "Characterization of the continuous, differentiating myeloid cell line (HL-60) from a patient with acute promyelocytic leukemia". Blood 54 (3): 713–733. 1979. doi:10.1182/blood.V54.3.713.713. PMID 288488. http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=288488.[yes|permanent dead link|dead link}}]
- ↑ Dalton WT, Jr; Ahearn, MJ; McCredie, KB; Freireich, EJ; Stass, SA; Trujillo, JM (January 1988). "HL-60 cell line was derived from a patient with FAB-M2 and not FAB-M3.". Blood 71 (1): 242–7. doi:10.1182/blood.V71.1.242.242. PMID 3422031.
- ↑ Breitman, T, S. Collins, B. Keene (1980). "Replacement of serum by insulin and transferrin supports growth and differentiation of the human promyelocytic leukemia cell line, HL-60.". Exp. Cell Res. 126 (2): 494–498. doi:10.1016/0014-4827(80)90296-7. PMID 6988226.
- ↑ Sugimoto, K, K. Yamada, M. Egashira, Y. yazaki, H. Hirai, A. Kikuchi and K. Oshimi (1998). "Temporal and Spatial Distribution of DNA Topoisomerase II Alters During Proliferation, Differentiation, and Apoptosis in HL-60 Cells.". Blood 91 (4): 1407–1417. doi:10.1182/blood.V91.4.1407. PMID 9454772.
- ↑ Ratanachoo, K., Gascoyne, P.R.C. and Ruchirawat, M. (2002). "Detection of cellular responses to toxicants by dielectrophoresis.". Biochim. Biophys. Acta 1564 (2): 449–458. doi:10.1016/S0005-2736(02)00494-7. PMID 12175928.
- ↑ González D., Bejarano I., Barriga C., Rodríguez A.B., Pariente J.A. (2010). "Oxidative Stress-Induced Caspases are Regulated in Human Myeloid HL-60 Cells by Calcium Signal". Current Signal Transduction Therapy 5 (2): 181–186. doi:10.2174/157436210791112172. http://www.eurekaselect.com/85761/article/oxidative-stress-induced-caspases-are-regulated-human-myeloid-hl-60-cells-calcium/.
- ↑ Teif V.B., Mallm J.P., Sharma T., Mark Welch D.B., Rippe K., Eils R., Langowski J., Olins A.L., Olins D.E. (2017). "Nucleosome repositioning during differentiation of a human myeloid leukemia cell line.". Nucleus 8 (2): 188–204. doi:10.1080/19491034.2017.1295201. PMID 28406749.
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