Evidence map›Paper›PMID 39910335›Full record

ArticleCellular & molecular immunology2025

Cell-associated galectin 9 interacts with cytotoxic T cells confers resistance to tumor killing in nasopharyngeal carcinoma through autophagy activation.

Ngar-Woon Kam, Cho Yiu Lau, Jeffrey Yan Ho Lau, Xin Dai, Yusi Liang, Syrus Pak Hei Lai, Michael King Yung Chung, Valen Zhuoyou Yu, Wenting Qiu, Mengsu Yang and 7 more

Abstract read
In one paragraph

Article in Cellular & molecular immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Galectin-9-An Emerging Glyco-Immune Checkpoint Target for Cancer Therapy.International journal of molecular sciences · 2025
    Review
  11. Review
  12. Article
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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

17 authors.

Ngar-Woon KamDepartment of Clinical Oncology, Centre of Cancer Medicine, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Cho Yiu LauDepartment of Clinical Oncology, Centre of Cancer Medicine, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Jeffrey Yan Ho LauLKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Xin DaiLaboratory of Synthetic Chemistry and Chemical Biology Limited, Hong Kong, China.
Yusi LiangLKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Syrus Pak Hei LaiLKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Michael King Yung ChungLKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.ORCID 0009-0004-4983-5233
Valen Zhuoyou YuDepartment of Clinical Oncology, Centre of Cancer Medicine, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Wenting QiuDepartment of Biomedical Sciences and Tung Biomedical Sciences Centre, City University of Hong Kong, Hong Kong, China.
Mengsu YangDepartment of Biomedical Sciences and Tung Biomedical Sciences Centre, City University of Hong Kong, Hong Kong, China.
Corey SmithQIMR Centre for Immunotherapy and Vaccine Development and Department of Immunology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.ORCID 0000-0002-7550-9595
Rajiv KhannaQIMR Centre for Immunotherapy and Vaccine Development and Department of Immunology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Kwan Ming NgLaboratory of Synthetic Chemistry and Chemical Biology Limited, Hong Kong, China.
Wei DaiDepartment of Clinical Oncology, Centre of Cancer Medicine, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Chi Ming CheLaboratory of Synthetic Chemistry and Chemical Biology Limited, Hong Kong, China.
Victor Ho-Fun LeeDepartment of Clinical Oncology, Centre of Cancer Medicine, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China. vhflee@hku.hk.ORCID 0000-0002-6283-978X
Dora L W KwongDepartment of Clinical Oncology, Centre of Cancer Medicine, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China. dlwkwong@hku.hk.

Funding

Food and Health Bureau of the Government of the Hong Kong Special Administrative Region | Health and Medical Research Fund (HMRF) 06172156
6 · The paper itself

Abstract

Immune effector cells, including cytotoxic T lymphocytes (CTLs) play essential roles in eliminating cancer cells. However, their functionality is often compromised, even when they infiltrate the tumor microenvironment (TME) or are transferred to cancer patients adoptively. In this study, we focused on galectin 9 (G9), an inhibitory ligand that we observed to be predominately positioned on the plasma membrane and readily interacts with CD8 + CTL in the TME of nasopharyngeal carcinoma (NPC). We discovered that cell-cell contact between activated effector CTLs and target tumor cells (TarTC) with G9 overexpression led to cellular death defects. Despite the formation of CTL-TarTC conjugates, there is no impact on the cell number nor viability of CTL, and the release of cytolytic content and associated activity were not completely abrogated. Instead, this interaction promoted autophagy and restricted necrosis in the TarTC. Furthermore, reducing G9 expression in tumor cells enhanced the suppressive effect on tumor growth upon adoptive transfer of activated effector CTL. Additionally, inhibiting autophagy effectively controlled tumor growth in cases of G9 overexpression. Therefore, we highlight the contribution of G9 in facilitating the resistance of NPC to CTL-mediated killing by inducing a selection-cell death state in tumor cells, characterized by increased autophagy and decreased necrosis.

Indexed as

AutophagyGalectinsNasopharyngeal CarcinomaNasopharyngeal NeoplasmsT-Lymphocytes, CytotoxicAnimalsCell Line, TumorCytotoxicity, ImmunologicHumansMiceTumor MicroenvironmentGalectinsLGALS9 protein, humanCell deathCytotoxic T cellsGalectin 9ImmunotherapyNasopharyngeal carcinomaTumor microenvironment

Identifiers

PMID39910335
PMCPMC11868493

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.