Evidence map›Paper›PMID 40641998›Full record

ArticleFrontiers in pharmacology2025

Galectin-9 treatment is cytotoxic for B cell lymphoma by disrupting autophagy.

Lisanne Koll, Harm Jan Lourens, Glenn Marsman, Stan de Haan, Toshiro Niki, Gerwin A Huls, Edwin Bremer, Valerie R Wiersma

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PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

1 citing paper in PubMed.

  1. Review
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

8 authors.

Lisanne KollDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Harm Jan LourensDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Glenn MarsmanDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Stan de HaanDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Toshiro NikiDepartment of Immunology, Kagawa University, Takamatsu, Kagawa, Japan.
Gerwin A HulsDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Edwin BremerDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.
Valerie R WiersmaDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The main cause of death for patients with non-Hodgkin lymphoma (NHL) remains therapy resistant relapses. Chemoresistance is commonly associated with apoptosis defects and upregulated autophagy. Therefore, novel therapeutic options that do not rely on apoptosis and target autophagy would be of interest to treat NHL. An agent that may fulfill these requirements is the glycan-binding protein Galectin-9 (Gal-9). Methods: A panel of B cell lymphoma NHL cell lines, including diffuse large B cell lymphoma (DLBCL), mantle cell lymphoma (MCL), Burkitt's lymphoma (BL), and (chemoresistant) follicular lymphoma (FL), were treated with Gal-9 after which cell counts and cell viability were determined. Basal mRNA and protein expression levels were respectively determined by RTqPCR and western blot. The impact of Gal-9 treatment on the autophagy pathway was determined using lysotracker, Cyto-ID and western blot (targeting LAMP2, p62, LC3B-I/LC3B-II). Results: Treatment with Gal-9 reduced total cell counts and cell viability of various DLBCL, MCL, BL and FL cell lines. Gal-9-induced cell death was associated with the inhibition of autophagy, as demonstrated by the accumulation of LC3B-II and p62. In addition, Gal-9-sensitive cells expressed lower basal protein levels of LC3B-I as compared to cells that responded less to this lectin. Furthermore, Gal-9 was cytotoxic for chemoresistant Sc-1 cells (Sc-1-RES), which were even more sensitive toward Gal-9 treatment than the parental cells (Sc-1-PAR). Conclusion: Gal-9 is a potent inducer of B cell lymphoma cell dead by inhibiting the proper execution of autophagy.

Indexed as

autophagyB cell lymphomacell deathchemoresistancegalectin-9 (Gal-9)

Identifiers

PMID40641998
PMCPMC12241159

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