Biomedical Science Letters (대한의생명과학회지)

The Korean Society for Biomedical Laboratory Sciences (대한의생명과학회)
권호 표지
DOI QR코드

DOI QR Code

Pro-apoptotic Effects of S100A8 and S100A9 on human FIP1L1-PDGFRα+ Eosinophilic Leukemia Cells

  • Lee, Ji-Sook (Department of Clinical Laboratory Science, Wonkwang Health Science University)
  • Received : 2021.04.16
  • Accepted : 2021.06.14
  • Published : 2021.06.30
Download PDF
⟨ Previous Next ⟩

Abstract

The S100 family proteins act as inducers of cancer cell apoptosis and inflammatory mediators. This study examined the pro-apoptotic mechanism caused by S100A8 and S100A9 in human FIP1L1-PDGFRα-positive eosinophilic leukemia cells. S100A8 and S100A9 elicited the death of EoL-1 cells in a time and dose-dependent manner. The activation of PDGFRα was suppressed by a decrease in PDGFRα after treatment with S100A8 and S100A9. Cycloheximide, a translation inhibitor, suppressed PDGFRα expression from 1 h to 5 h, and a co-treatment with S100A8 and S100A9 boosted the decrease in expression. The phosphorylation and expression of STAT5 decreased after treatment with S100A8 and S100A9 in EoL-1 and imatinib-resistant (EoL-1-IR) cells. S100A8 and S100A9 induced the chemotaxis of EoL-1 cells but did not affect the chemoattraction of EoL-1-IR. These findings indicate the cell death mechanism due to S100 family proteins and the development of leukemia therapy using S100A8 and S100A9.

Keywords

Acknowledgement

This paper was supported by Wonkwang Health Science University in 2021.

References

  1. Bresnick, AR, Weber DJ, Zimmer DB. S100 proteins in cancer. Nature Review Cancer. 2015. 15: 96-109. https://doi.org/10.1038/nrc3893
  2. Donato R, Cannon BR, Sorci G, et al. Functions of S100 proteins. Current Molecular Medicine. 2013. 13: 24-57. https://doi.org/10.2174/156652413804486214
  3. Goyette J, Geczy CL. Inflammation-associated S100 proteins: new mechanisms that regulate function. Amino Acids. 2011. 41: 821-842. https://doi.org/10.1007/s00726-010-0528-0
  4. Kim IS, Jang SW, Sung HJ, Lee JS, Ko J. Differential CCR1-mediated chemotaxis signaling induced by human CC chemokine HCC-4/CCL16 in HOS cells. FEBS Letters. 2005. 579: 6044-6048. https://doi.org/10.1016/j.febslet.2005.09.064
  5. Kim IS, Lee JS. S100A8 and S100A9 secreted by allergens in monocytes inhibit spontaneous apoptosis of normal and asthmatic neutrophils via the Lyn/akt/ERK pathway. Korean Journal of Clinical Laboratory Science. 2017. 49: 128-134. https://doi.org/10.15324/kjcls.2017.49.2.128
  6. Kim IS, Lee JS. The pro-apoptotic effects of S100A8 and S100A9 in human monocytic leukemia cells, THP-1. Biomedical Science Letters. 2018. 24: 134-137. https://doi.org/10.15616/BSL.2018.24.2.134
  7. Lambert F, Heimann P, Herens C, Chariot A, Bours V. A case of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia with a rare FIP1L1 breakpoint. Journal of Molecular Diagnostics. 2007. 9: 414-419. https://doi.org/10.2353/jmoldx.2007.060196
  8. Lee JS, Lee NR, Kashif A, et al. S100A8 and S100A9 promote apoptosis of chronic eosinophilic leukemia cells. Frontiers in Immuology. 2020. 11: 1258. https://doi.org/10.3389/fimmu.2020.01258
  9. Qu SQ, Qin TJ, Xu ZF, et al. Long-term outcomes of imatinib in patients with FIP1L1/ PDGFRA associated chronic eosinophilic leukemia: experience of a single center in China. Oncotarget. 2016. 7: 33229-33236. https://doi.org/10.18632/oncotarget.8906
  10. Sung KH, Kim IS, Lee JS. Different protein expression between human eosinophilic leukemic cells, EoL-1 and imatinibresistant EoL-1 cells, EoL-1-IR. Biomedical Science Letters. 2018. 24: 426-429. https://doi.org/10.15616/BSL.2018.24.4.426
  11. Wu Y, Chen C, Sun X, Shi X. Cyclin-dependent kinase 7/9 inhibitor SNS-032 abrogates FIP1-like-1 platelet-derived growth factor receptor α and bcr-abl oncogene addiction in malignant hematologic cells. Clinical Cancer Research. 2012. 18: 1966-1978. https://doi.org/10.1158/1078-0432.CCR-11-1971