Evaluating T-Cell Immunoglobulin Mucin-3 (TIM-3) Receptor in the Growth Inhibition of Acute Lymphoblastic Leukemia (ALL) Cell Lines

Document Type : Original Article (s)

Authors

1 MSc Student, Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences AND Student Research Committee, Isfahan University of Medical Sciences, Isfahan, Iran

2 Assistant Professor, Monoclonal Antibody Research Center, Avicenna Research Institute, The Academic Center for Education, Culture and Research (ACECR), Tehran, Iran

3 PhD Student, Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran

4 Monoclonal Antibody Research Center, Avicenna Research Institute, The Academic Center for Education, Culture and Research (ACECR), Tehran, Iran

5 Assistant Professor, Department of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences AND Pharmaceutical Sciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

Abstract

Background: T-cell immunoglobulin-mucin (TIM) is a cell-surface and transmembrane glycoprotein. TIM-3 plays a pivotal role in proliferation, invasion and metastasis of tumor cells. The present study was designed to evaluate the expressions of the TIM-3 and the role of the galectin-9, as TIM-3 ligand, in the regulation of cell proliferation in human acute lymphoblastic leukemia (ALL) cell lines.Methods: The expression level of TIM-3 was examined in the Jurkat and KE-37 cell lines using real-time polymerase chain reaction method. MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium] viability test was used to study the cell proliferation effect of galectin-9.Findings: TIM-3 mRNAs were detected in the both Jurkat and KE-37 cell lines. The expression of TIM-3 in Jurkat cell line was higher than KE-37 cell line (P < 0.001). The MTS assay revealed that galectin-9 reduced cells proliferation in a dose-dependent manner (> 1 nM) in the both cell lines (P < 0.050).Conclusion: The present investigation introduced a possible mechanism for the control of acute lymphoblastic leukemia cell proliferation through TIM-3 and demonstrated that galectin-9 can inhibit the proliferation of Jurkat and KE-37 cell lines.

Keywords

References

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Journal of Isfahan Medical School
Volume 33, Issue 345 - Serial Number 345
July and August 2015
Pages 1250-1260

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History

  • Receive Date: 06 May 2015
  • Revise Date: 01 November 2024
  • Accept Date: 06 April 2022

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