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Galectin-9 Inhibits Cell Proliferation and Induces Apoptosis in Jurkat and Ke-37 Acute Lymphoblastic Leukemia Cell Lines Via Caspase-3 Activation Publisher



Zargar Balajam N1 ; Shabani M2 ; Aghaei M1
Authors
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Authors Affiliations
  1. 1. Department of Clinical Biochemistry and Isfahan Pharmaceutical Sciences Research Center, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Source: Research in Pharmaceutical Sciences Published:2021


Abstract

Background and purpose: Acute lymphoblastic leukemia (ALL) is a type of cancer of blood and bone marrow characterized by abnormal proliferation of lymphoid progenitor cells. Galectin-9 is a tandem-repeat type galectin expressed in various tumor cells. It seems that the connection between galectin-9 and T cell immunoglobulin mucin-3 receptor acts as a negative regulator of cancer cells proliferation. Experimental approach: In this research, the effects of galectin-9 were investigated using MTS cell proliferation colorimetric, colony-forming, annexin V-FITC/PI, and caspase-3 assays in the Jurkat and KE-37 cell lines of ALL. Furthermore, the western blotting technique was used to evaluate the levels of apoptotic proteins such as Bax and Bcl-2 in these cell lines. Findings/Results: Our results indicated that galectin-9 can considerably reduce the cell growth and colony formation ability of both Jurkat and KE-37 cell lines in a concentration-dependent manner. Besides, galectin-9 induced apoptosis in a concentration-dependent manner in ALL cells by a mechanism associated with Bax/Bcl-2 expression and activation of the caspase-3 activation. Conclusion and implications: Galectin-9 inhibited the growth and proliferation of cell lines with increased programmed cell death, therefore it can be considered as a potential factor in the progression of ALL therapeutics that needs more research in this context. © 2021 Wolters Kluwer Medknow Publications. All rights reserved.
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