ArticleThe American journal of pathology2013
Surfactant protein A suppresses lung cancer progression by regulating the polarization of tumor-associated macrophages.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 62 citations in OpenAlex.
- Single-cell dissection reveals immunosuppressive F13A1+ macrophage as a hallmark for multiple primary lung cancers.Clinical and translational medicine · 2024Article
- The Role of Pulmonary Collectins, Surfactant Protein A (SP-A) and Surfactant Protein D (SP-D) in Cancer.Cancers · 2024Review
- Anti-tumor activity of a recombinant measles virus against canine lung cancer cells.Scientific reports · 2023Article
- Candidate pathway analysis of surfactant proteins identifies CTSH and SFTA2 that influences lung cancer risk.Human molecular genetics · 2023Article
- Construction of an endoplasmic reticulum stress-related signature in lung adenocarcinoma by comprehensive bioinformatics analysis.BMC pulmonary medicine · 2023Article
- Modulation of natural killer cell exhaustion in the lungs: the key components from lung microenvironment and lung tumor microenvironment.Frontiers in immunology · 2023Review
- USP15 negatively regulates lung cancer progression through the TRAF6-BECN1 signaling axis for autophagy induction.Cell death & disease · 2022Article
- SFTPA1 is a potential prognostic biomarker correlated with immune cell infiltration and response to immunotherapy in lung adenocarcinoma.Cancer immunology, immunotherapy : CII · 2022Article
- The Lung Alveolar Cell (LAC) miRNome and Gene Expression Profile of the SP-A-KO Mice After Infection With and Without Rescue With Human Surfactant Protein-A2 (1AFrontiers in immunology · 2022Article
- The importance of enhancer methylation for epigenetic regulation of tumorigenesis in squamous lung cancer.Experimental & molecular medicine · 2022Article
- CXCR4 Knockdown Via CRISPR/CAS9 in a Tumor-Associated Macrophage Model Decreases Human Breast Cancer Cell Migration.Cureus · 2021Article
- Characterizing Macrophage Diversity in Metastasis-Bearing Lungs Reveals a Lipid-Associated Macrophage Subset.Cancer research · 2021Article
- Surfactant Protein A, a Novel Regulator for Smooth Muscle Phenotypic Modulation and Vascular Remodeling-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Article
- Review
- Dexamethasone Treatment Increases the Intracellular Calcium Level ThroughInternational journal of molecular sciences · 2020Article
- Sex-Specific Regulation of Gene Expression Networks by Surfactant Protein A (SP-A) Variants in Alveolar Macrophages in Response toFrontiers in immunology · 2020Article
- Pulmonary-Affinity Paclitaxel Polymer Micelles in Response to Biological Functions of Ambroxol Enhance Therapeutic Effect on Lung Cancer.International journal of nanomedicine · 2020Article
- The Crosstalk Between Tumor-Associated Macrophages (TAMs) and Tumor Cells and the Corresponding Targeted Therapy.Frontiers in oncology · 2020Review
- The Tumor-Associated Macrophage-M2-Cancer Cell Complex and the Observation of Heterogeneous Modification of the Morphological Structure of Lung Adenocarcinoma.OncoTargets and therapy · 2020Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Surfactant protein A (SP-A) is a large multimeric protein found in the lungs. In addition to its immunoregulatory function in infectious respiratory diseases, SP-A is also used as a marker of lung adenocarcinoma. Despite the finding that SP-A expression levels in cancer cells has a relationship with patient prognosis, the function of SP-A in lung cancer progression is unknown. We investigated the role of SP-A in lung cancer progression by introducing the SP-A gene into human lung adenocarcinoma cell lines. SP-A gene transduction suppressed the progression of tumor in subcutaneous xenograft or lung metastasis mouse models. Immunohistochemical analysis showed that the number of M1 antitumor tumor-associated macrophages (TAMs) was increased and the number of M2 tumor-promoting TAMs was not changed in the tumor tissue produced by SP-A-expressing cells. In addition, natural killer (NK) cells were also increased and activated in the SP-A-expressing tumor. Moreover, SP-A did not inhibit tumor progression in mice depleted of NK cells. Taking into account that SP-A did not directly activate NK cells, these results suggest that SP-A inhibited lung cancer progression by recruiting and activating NK cells via controlling the polarization of TAMs.
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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.