HL60 explained

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. 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. Gallagher R, Collins S, Trujillo J, etal . Characterization of the continuous, differentiating myeloid cell line (HL-60) from a patient with acute promyelocytic leukemia . . 54 . 3 . 713–733 . 1979 . 10.1182/blood.V54.3.713.713 . 288488 . free .
  2. Dalton WT. Jr. Ahearn. MJ. McCredie. KB. Freireich. EJ. Stass. SA. Trujillo. JM. HL-60 cell line was derived from a patient with FAB-M2 and not FAB-M3.. Blood. January 1988. 71. 1. 242–7. 10.1182/blood.V71.1.242.242 . 3422031. free.
  3. 10.1016/0014-4827(80)90296-7 . 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 . 6988226.
  4. 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 . 10.1182/blood.V91.4.1407 . 9454772. free .
  5. 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 . 12175928 . 2726261 . 10.1016/S0005-2736(02)00494-7.
  6. 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 . 10.2174/157436210791112172 .
  7. Teif V.B., Mallm J.P., Sharma T., Mark Welch D.B., Rippe K., Eils R., Langowski J., Olins A.L., Olins D.E. . Nucleosome repositioning during differentiation of a human myeloid leukemia cell line. . Nucleus . 8 . 2 . 188–204 . 2017. 28406749 . 10.1080/19491034.2017.1295201 . 5403151.

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