ArticleCellular and molecular life sciences : CMLS2021
GRP78 facilitates M2 macrophage polarization and tumour progression.
Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- GRP78 dysregulation: A proposed molecular mechanism linking the tumor microenvironment to sepsis susceptibility in patients with cancer (Review).International journal of molecular medicine · 2026Review
- GRP78 in viral pneumonia: dual regulatory mechanisms and translational prospects.Clinical and experimental medicine · 2026Review
- Macrophages in lung cancer: principal factors, regulatory mechanisms, and therapeutic opportunities: a narrative review.Translational lung cancer research · 2026Review
- TCF12-mediated transcriptional activation of CCDC34 is involved in the positive feedback of tumor-associated macrophages and EMT to promote LUSC.Cell biology and toxicology · 2026Article
- Article
- Ginkgetin targets GRP78 to induce dual pathways of ER stress and immune activation in osteosarcoma.Oncogene · 2026Article
- Association between four indirect indicators of insulin resistance and lung cancer: evidence from UK biobank and Mendelian randomization analysis.BMC cancer · 2026Article
- NScience China. Life sciences · 2026Article
- Endoplasmic Reticulum Stress in Cancer.MedComm · 2025Review
- GRP78 as a potential therapeutic target in cancer treatment: an updated review of its role in chemoradiotherapy resistance of cancer cells.Medical oncology (Northwood, London, England) · 2025Review
- Exosome-derived proteins in gastric cancer progression, drug resistance, and immune response.Cellular & molecular biology letters · 2024Review
- [Progress in the Study of Mechanisms Clinically Relevant to Insulin Resistance and Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Review
- Inhibition of STAT3: A promising approach to enhancing the efficacy of chemotherapy in medulloblastoma.Translational oncology · 2024Review
- Extracellular Interactors of the IGF System: Impact on Cancer Hallmarks and Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Research advances on signaling pathways regulating the polarization of tumor-associated macrophages in lung cancer microenvironment.Frontiers in immunology · 2024Review
- Prognostic and immunotherapeutic significances of M2 macrophage-related genes signature in lung cancer.Journal of Cancer · 2024Article
- Macrophage neogenin deficiency exacerbates myocardial remodeling and inflammation after acute myocardial infarction through JAK1-STAT1 signaling.Cellular and molecular life sciences : CMLS · 2023Article
- An iRGD-conjugated photothermal therapy-responsive gold nanoparticle system carrying siCDK7 induces necroptosis and immunotherapeutic responses in lung adenocarcinoma.Bioengineering & translational medicine · 2023Article
- New progresses on cell surface protein HSPA5/BiP/GRP78 in cancers and COVID-19.Frontiers in immunology · 2023Review
- Advances in the role of STAT3 in macrophage polarization.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
This study investigated the regulation of GRP78 in tumour-associated macrophage polarization in lung cancer. First, our results showed that GRP78 was upregulated in macrophages during M2 polarization and in a conditioned medium derived from lung cancer cells. Next, we found that knocking down GRP78 in macrophages promoted M1 differentiation and suppressed M2 polarization via the Janus kinase/signal transducer and activator of transcription signalling. Moreover, conditioned medium from GRP78- or insulin-like growth factor 1-knockdown macrophages attenuated the survival, proliferation, and migration of lung cancer cells, while conditioned medium from GRP78-overexpressing macrophages had the opposite effects. Additionally, GRP78 knockdown reduced both the secretion of insulin-like growth factor 1 and the phosphorylation of the insulin-like growth factor 1 receptor. Interestingly, insulin-like growth factor 1 neutralization downregulated GRP78 and suppressed GRP78 overexpression-induced M2 polarization. Mechanistically, insulin-like growth factor 1 treatment induced the translocation of GRP78 to the plasma membrane and promoted its association with the insulin-like growth factor 1 receptor. Finally, IGF-1 blockade and knockdown as well as GRP78 knockdown in macrophages inhibited M2 macrophage-induced survival, proliferation, and migration of lung cancer cells both in vitro and in vivo.
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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.