ArticleResearch in pharmaceutical sciences2021
Galectin-9 inhibits cell proliferation and induces apoptosis in Jurkat and KE-37 acute lymphoblastic leukemia cell lines
Article in Research in pharmaceutical sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Galectin-9 induces IL-1β production as a key inflammatory cytokine in the acute myeloid leukemia cell line (U937).Research in pharmaceutical sciences · 2025Article
- Galectins-1, -3 and -9 in leukemia: mechanistic insights and therapeutic translation.Frontiers in immunology · 2025Review
- α2β1 Integrin specific inhibitor BTT-3033 promotes paclitaxel-induced apoptosis in human ovarian cancer cells.Research in pharmaceutical sciences · 2024Article
- The regulating role of galectin-9 in immune cell populations.Frontiers in pharmacology · 2024Review
- Single-cell RNA sequencing uncovers molecular mechanisms of intravenous immunoglobulin plus methylprednisolone in Kawasaki disease: attenuated monocyte-driven inflammation and improved NK cell cytotoxicity.Frontiers in immunology · 2024Article
- Galectin-9 has non-apoptotic cytotoxic activity toward acute myeloid leukemia independent of cytarabine resistance.Cell death discovery · 2023Article
- Galectin-9 and myeloid-derived suppressor cell as prognostic indicators for chronic lymphocytic leukemia.Immunity, inflammation and disease · 2023Article
- Galectin functions in cancer-associated inflammation and thrombosis.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeAcute 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/
resultsOur 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.
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