ArticleAmerican journal of cancer research2023
Activation of the GPR35 on ILC2 drives immunosuppression to promote lung cancer progression.
Article in American journal of cancer research, 2023. 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, 6 citations in OpenAlex.
- Screening air pollutants-related genes to construct a prognostic risk model for lung adenocarcinoma and analyzing its immune microenvironment.Journal of thoracic disease · 2026Article
- Kynurenic Acid/GPR35 Signaling Protects the Infarcted Heart by Suppressing Macrophage mtDNA-Triggered cGAS-STING Activation.Antioxidants (Basel, Switzerland) · 2026Article
- The context-dependent role of group 2 innate lymphoid cells in lung diseases.Acta biochimica et biophysica Sinica · 2026Review
- Increased GPR35 expression is correlated with poor prognosis in prostate cancer.World journal of surgical oncology · 2025Article
- Cell components of tumor microenvironment in lung adenocarcinoma: Promising targets for small-molecule compounds.Chinese medical journal · 2025Review
- The power of many: Multilevel targeting of representative chemokine and metabolite GPCRs in personalized cancer therapy.European journal of immunology · 2024Review
- From orphan to oncogene: The role of GPR35 in cancer and immune modulation.Cytokine & growth factor reviews · 2024Review
- GPR35 acts a dual role and therapeutic target in inflammation.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is the most common cancer type with poor prognosis. While G protein-coupled receptor 35 (GPR35) is a potent stimulator of tumor growth, group 2 innate lymphoid cells (ILC2) have shown dual effects in tumorigenesis. Intriguingly, inflammation induced GPR35 activation leads to an upregulation in the markers associated with ILC2. Here, we reported that GPR35 knockout mice exhibited a significantly reduced tumor growth and altered immune infiltration in tumors. Furthermore, activating GPR35 in different mouse models promoted tumor development by enhancing the production of IL-5 and IL-13, thereby facilitating the formation of the ILC2-MDSC axis. Moreover, we found that GPR35 was a poor prognostic factor in patients with lung adenocarcinoma. Together, our findings suggest the potential application of targeting GPR35 in cancer immunotherapy.
Indexed as
Identifiers
37424810PMC10326596W4383710392What OpenQuestion holds
Registered trials
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.