Evidence map›Paper›PMID 38267906›Full record

ArticleBMC cancer2024

TIM-3/Galectin-9 interaction and glutamine metabolism in AML cell lines, HL-60 and THP-1.

Hooriyeh Shapourian, Mustafa Ghanadian, Nahid Eskandari, Abolfazl Shokouhi, Gülderen Yanikkaya Demirel, Alexandr V Bazhin, Mazdak Ganjalikhani-Hakemi

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Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 8 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 3 countries.

Hooriyeh ShapourianDepartment of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Mustafa GhanadianDepartment of Pharmacognosy, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran.
Nahid EskandariDepartment of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Abolfazl ShokouhiDepartment of Endocrine and metabolism research center, Isfahan University of Medical Sciences, Isfahan, Iran.
Gülderen Yanikkaya DemirelDepartment of Immunology, Faculty of Medicine, Yeditepe University, Istanbul, Turkey.
Alexandr V BazhinDepartment of General, Visceral and Transplant Surgery, Ludwig Maximilians University of Munich, Munich, Germany.
Mazdak Ganjalikhani-HakemiDepartment of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. mghakemi@med.mui.ac.ir.
Isfahan University of Medical Sciences · IRDeutschen Konsortium für Translationale Krebsforschung · DEIstanbul Medipol University · TRYeditepe University · TR

Funding

Isfahan University of Medical Sciences 3400961
6 · The paper itself

Abstract

backgroundT cell immunoglobulin and mucin-domain containing-3 (TIM-3) is a cell surface molecule that was first discovered on T cells. However, recent studies revealed that it is also highly expressed in acute myeloid leukemia (AML) cells and it is related to AML progression. As, Glutamine appears to play a prominent role in malignant tumor progression, especially in their myeloid group, therefore, in this study we aimed to evaluate the relation between TIM-3/Galectin-9 axis and glutamine metabolism in two types of AML cell lines, HL-60 and THP-1.

methodsCell lines were cultured in RPMI 1640 which supplemented with 10% FBS and 1% antibiotics. 24, 48, and 72 h after addition of recombinant Galectin-9 (Gal-9), RT-qPCR analysis, RP-HPLC and gas chromatography techniques were performed to evaluate the expression of glutaminase (GLS), glutamate dehydrogenase (GDH) enzymes, concentration of metabolites; Glutamate (Glu) and alpha-ketoglutarate (α-KG) in glutaminolysis pathway, respectively. Western blotting and MTT assay were used to detect expression of mammalian target of rapamycin complex (mTORC) as signaling factor, GLS protein and cell proliferation rate, respectively.

resultsThe most mRNA expression of GLS and GDH in HL-60 cells was seen at 72 h after Gal-9 treatment (p = 0.001, p = 0.0001) and in THP-1 cell line was observed at 24 h after Gal-9 addition (p = 0.001, p = 0.0001). The most mTORC and GLS protein expression in HL-60 and THP-1 cells was observed at 72 and 24 h after Gal-9 treatment (p = 0.0001), respectively. MTT assay revealed that Gal-9 could promote cell proliferation rate in both cell lines (p = 0.001). Glu concentration in HL-60 and α-KG concentration in both HL-60 (p = 0.03) and THP-1 (p = 0.0001) cell lines had a decreasing trend. But, Glu concentration had an increasing trend in THP-1 cell line (p = 0.0001).

conclusionTaken together, this study suggests TIM-3/Gal-9 interaction could promote glutamine metabolism in HL-60 and THP-1 cells and resulting in AML development.

Indexed as

GlutamineLeukemia, Myeloid, AcuteGalectinsGlutamic AcidHepatitis A Virus Cellular Receptor 2HL-60 CellsHumansGalectinsGlutamic AcidGlutamineHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2LGALS9 protein, humanAcute myeloid leukemia (AML)Galectin-9 (Gal-9)Glutamate dehydrogenase (GDH)Glutaminase (GLS)Glutamine metabolismT cell immunoglobulin and mucin-domain containing-3 (TIM-3)

Identifiers

PMID38267906
PMCPMC10809689
OpenAlexW4391160982

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.