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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
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...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Wolters Kluwer - Medknow
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8562407/ https://www.ncbi.nlm.nih.gov/pubmed/34760009 http://dx.doi.org/10.4103/1735-5362.327507 |
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author | Zargar Balajam, Narges Shabani, Mahdi Aghaei, Mahmoud |
author_facet | Zargar Balajam, Narges Shabani, Mahdi Aghaei, Mahmoud |
author_sort | Zargar Balajam, Narges |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8562407 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Wolters Kluwer - Medknow |
record_format | MEDLINE/PubMed |
spelling | pubmed-85624072021-11-09 Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines via caspase-3 activation Zargar Balajam, Narges Shabani, Mahdi Aghaei, Mahmoud Res Pharm Sci Original Article 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. Wolters Kluwer - Medknow 2021-10-15 /pmc/articles/PMC8562407/ /pubmed/34760009 http://dx.doi.org/10.4103/1735-5362.327507 Text en Copyright: © 2021 Research in Pharmaceutical Sciences https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Original Article Zargar Balajam, Narges Shabani, Mahdi Aghaei, Mahmoud Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines via caspase-3 activation |
title | Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines via caspase-3 activation |
title_full | Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines via caspase-3 activation |
title_fullStr | Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines via caspase-3 activation |
title_full_unstemmed | Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines via caspase-3 activation |
title_short | Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines via caspase-3 activation |
title_sort | galectin-9 inhibits cell proliferation and induces apoptosis in jurkat and ke-37 acute lymphoblastic leukemia cell lines via caspase-3 activation |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8562407/ https://www.ncbi.nlm.nih.gov/pubmed/34760009 http://dx.doi.org/10.4103/1735-5362.327507 |
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