Evidence map›Paper›PMID 37409887›Full record

ArticleCancer research2023

Galectin-1 Mediates Chronic STING Activation in Tumors to Promote Metastasis through MDSC Recruitment.

Dhanya K Nambiar, Vignesh Viswanathan, Hongbin Cao, Weiruo Zhang, Li Guan, Manish Chamoli, Brittany Holmes, Christina Kong, Rachel Hildebrand, Amanda Jeanette Koong and 6 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

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

39 citing papers in PubMed, 38 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

16 authors at 5 institutions in 2 countries.

Dhanya K NambiarDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0002-0648-403X
Vignesh ViswanathanDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0001-8307-9508
Hongbin CaoDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0001-8596-3268
Weiruo ZhangDepartment of Biomedical Data Science, Stanford University School of Medicine, Stanford, California.ORCID 0000-0003-3680-7562
Li GuanDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0003-4419-8170
Manish ChamoliBuck Institute for Research on Aging, Novato, California.ORCID 0000-0003-0339-7894
Brittany HolmesDepartment of Pathology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0003-3374-050X
Christina KongDepartment of Pathology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0003-2098-6842
Rachel HildebrandDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0001-6568-347X
Amanda Jeanette KoongDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0002-2447-4695
Rie von EybenDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0003-2355-8667
Sylvia PlevritisDepartment of Biomedical Data Science, Stanford University School of Medicine, Stanford, California.ORCID 0000-0003-2796-9180
Lingyin LiDepartment of Biochemistry; Program in Chemistry, Engineering, and Medicine for Human Health (ChEM-H), Stanford University, Stanford, California.ORCID 0000-0003-4386-7926
Amato GiacciaDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0002-9469-1388
Edgar EnglemanDepartment of Pathology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0002-2096-9279
Quynh Thu LeDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California.ORCID 0000-0002-3682-1439
Stanford Medicine · USBuck Institute for Research on Aging · USCRUK/MRC Oxford Institute for Radiation Oncology · GBStanford Health Care · USStanford University · US

Funding

NRG Oncology Network Group Operations Center - GY9 BIQSFP Reports/BudgetsU10CA180868 · NCI · NRG ONCOLOGY FOUNDATION, INC. · PI Quynh-Thu Xuan Le, ROBERT S. MANNEL · 2014 to 2026
$206.8M
Translational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI MICHAEL KENNEY · 2007 to 2026
$71.4M
Translational Biology CoreP01CA257907 · NCI · STANFORD UNIVERSITY · PI Quynh-Thu Xuan Le · 2022 to 2026
$12.0M
Systems Biology of Tumor-Immune-Stromal Interactions in Metastatic ProgressionU54CA274511 · NCI · STANFORD UNIVERSITY · PI EDGAR G. ENGLEMAN, SYLVIA KATINA PLEVRITIS · 2023 to 2026
$9.5M
Precision imaging for risk stratification and personalized therapy of oropharyngeal cancerR01DE030894 · NIDCR · STANFORD UNIVERSITY · PI Quynh-Thu Xuan Le, Ruijiang Li · 2022 to 2026
$3.0M
The role of Galectin-1 in shaping the immune suppressive landscape in head and neck cancerR01DE029672 · NIDCR · STANFORD UNIVERSITY · PI LE, QUYNH-THU XUAN · 2021 to 2025
$2.9M
Salivary gland response to Desert hedgehog signaling as an antidote to damage from therapeutic radiationR01DE031724 · NIDCR · STANFORD UNIVERSITY · PI PHILIP A BEACHY · 2022 to 2026
$2.5M
Medical Research Council MC_UU_00001/8NCI NIH HHS P01 CA257907NCI NIH HHS P30 CA124435NCI NIH HHS U10 CA180868NCI NIH HHS U54 CA274511NIDCR NIH HHS R01 DE029672NIDCR NIH HHS R01 DE030894NIDCR NIH HHS R01 DE031724NIH HHS R01DE031724
6 · The paper itself

Abstract

The immune system plays a crucial role in the regulation of metastasis. Tumor cells systemically change immune functions to facilitate metastatic progression. Through this study, we deciphered how tumoral galectin-1 (Gal1) expression shapes the systemic immune environment to promote metastasis in head and neck cancer (HNC). In multiple preclinical models of HNC and lung cancer in immunogenic mice, Gal1 fostered the establishment of a premetastatic niche through polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC), which altered the local microenvironment to support metastatic spread. RNA sequencing of MDSCs from premetastatic lungs in these models demonstrated the role of PMN-MDSCs in collagen and extracellular matrix remodeling in the premetastatic compartment. Gal1 promoted MDSC accumulation in the premetastatic niche through the NF-κB signaling axis, triggering enhanced CXCL2-mediated MDSC migration. Mechanistically, Gal1 sustained NF-κB activation in tumor cells by enhancing stimulator of interferon gene (STING) protein stability, leading to prolonged inflammation-driven MDSC expansion. These findings suggest an unexpected protumoral role of STING activation in metastatic progression and establish Gal1 as an endogenous-positive regulator of STING in advanced-stage cancers. SIGNIFICANCE: Galectin-1 increases STING stability in cancer cells that activates NF-κB signaling and CXCL2 expression to promote MDSC trafficking, which stimulates the generation of a premetastatic niche and facilitates metastatic progression.

Indexed as

Lung NeoplasmsMyeloid-Derived Suppressor CellsAnimalsGalectin 1MiceNF-kappa BSignal TransductionSTING ProteinTumor MicroenvironmentGalectin 1NF-kappa BSting1 protein, mouseSTING Protein

Identifiers

PMID37409887
PMCPMC10592379
OpenAlexW4383302326

What OpenQuestion holds

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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 OpenQuestion graph.