ArticleCancer research2011
Api6/AIM/Spα/CD5L overexpression in alveolar type II epithelial cells induces spontaneous lung adenocarcinoma.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 64 citations in OpenAlex.
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- A feature selection-based framework to identify biomarkers for cancer diagnosis: A focus on lung adenocarcinoma.PloS one · 2022Article
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- Association between apoptosis inhibitor of macrophage and microsatellite instability status in colorectal cancer.BMC gastroenterology · 2020Article
- CD5L-induced activation of autophagy is associated with hepatoprotection in ischemic reperfusion injury via the CD36/ATG7 axis.Experimental and therapeutic medicine · 2020Article
- MiR-1307-5p targeting TRAF3 upregulates the MAPK/NF-κB pathway and promotes lung adenocarcinoma proliferation.Cancer cell international · 2020Article
- Bacterial DNA induces the formation of heat-resistant disease-associated proteins in human plasma.Scientific reports · 2019Observational
- The effect of exposure time and concentration of airborne PMRedox biology · 2019Article
- CD5L is a pleiotropic player in liver fibrosis controlling damage, fibrosis and immune cell content.EBioMedicine · 2019Article
- Transthyretin Stimulates Tumor Growth through Regulation of Tumor, Immune, and Endothelial Cells.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- CD5L Promotes M2 Macrophage Polarization through Autophagy-Mediated Upregulation of ID3.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Chronic inflammation is an important contributor to the development of lung cancers, one of the most common malignancies worldwide, but the underlying molecular mechanisms of inflammation that specifically cue cancer risk remain poorly understood. Apoptosis inhibitor 6 (Api6, also known as AIM, Sp-α, and CD5L) is a downstream target gene of neutral lipids and peroxisome proliferator-activated receptor gamma in lung alveolar type II (AT II) epithelial cells. An association among increased expression of Api6 in certain settings of pathogenic lung inflammation in mice prompted us to hypothesize a possible role in cancer. Here, we report that Api6 promotes malignant transformation by limiting lung epithelial cell apoptosis and promoting immune escape. The specific function of Api6 in AT II cells was determined by using a doxycycline-inducible Api6 mouse model. Api6 overexpression inhibited apoptosis and activated oncogenic signaling in AT II lung epithelial cells, inducing emphysema and adenocarcinoma. In addition, Api6 overexpression in AT II cells increased the concentrations of proinflammatory cytokines/chemokines in bronchoalveolar lavage fluid and serum, promoting expansion of myeloid-derived suppressor cells (MDSC) in lung and blood but not in bone marrow or spleen. Lung MDSCs suppressed T-cell proliferation and activity in vitro and reduced levels of T cells in vivo following doxycycline treatment to activate Api6. Together, our findings establish that Api6 promotes lung tumorigenesis by blocking a mechanism of epithelial apoptosis that would normally support immunosurveillance.
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