ArticleOncogene2015
SAA1 polymorphisms are associated with variation in antiangiogenic and tumor-suppressive activities in nasopharyngeal carcinoma.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Integrated Plasma and Tumor Proteomics of Nasopharyngeal Carcinoma in a Moroccan Cohort.International journal of molecular sciences · 2025Article
- Recent Advances in Studies of Serum Amyloid A: Implications in Inflammation, Immunity and Tumor Metastasis.International journal of molecular sciences · 2025Review
- Prediction of clear cell renal cell carcinoma prognosis based on an immunogenomic landscape analysis.Heliyon · 2024Article
- Acute-serum amyloid A and A-SAA-derived peptides as formyl peptide receptor (FPR) 2 ligands.Frontiers in endocrinology · 2023Review
- Lipocalin-2 negatively regulates epithelial-mesenchymal transition through matrix metalloprotease-2 downregulation in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022Article
- Serum Extracellular Vesicle Stratifin Is a Biomarker of Perineural Invasion in Patients With Colorectal Cancer and Predicts Worse Prognosis.Frontiers in oncology · 2022Article
- Fluorescent quenching probes basedHeliyon · 2021Article
- The Inhibitory Effects of Recombinant Hespintor Combined with Sorafenib on Transplanted Human Hepatoma in Nude Mice, and Transcriptional Regulation of Hespintor Based on RNA-Seq.Journal of Cancer · 2021Article
- SAA1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of AKT signaling.Journal of Cancer · 2021Article
- Loss of Down Syndrome Critical Region-1 Mediated-Hypercholesterolemia Accelerates Corneal Opacity Via Pathological Neovessel Formation.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Epigenetic remodelling shapes inflammatory renal cancer and neutrophil-dependent metastasis.Nature cell biology · 2020Article
- Serum amyloid A1 as a biomarker for radiation dose estimation and lethality prediction in irradiated mouse.Annals of translational medicine · 2019Article
- The anti-tumor function of the IKK inhibitor PS1145 and high levels of p65 and KLF4 are associated with the drug resistance in nasopharyngeal carcinoma cells.Scientific reports · 2019Article
- Serum amyloid A1 in combination with integrin αVβ3 increases glioblastoma cells mobility and progression.Molecular oncology · 2018Article
- Integrative analyses of transcriptome sequencing identify novel functional lncRNAs in esophageal squamous cell carcinoma.Oncogenesis · 2017Article
- Review
- The putative tumor activator ARHGEF3 promotes nasopharyngeal carcinoma cell pathogenesis by inhibiting cellular apoptosis.Oncotarget · 2016Article
- Novel lentiviral-inducible transgene expression systems and versatile single-plasmid reporters for in vitro and in vivo cancer biology studies.Cancer gene therapy · 2015Article
- Serum amyloid A1 isoforms display different efficacy at Toll-like receptor 2 and formyl peptide receptor 2.Immunobiology · 2014Article
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21 authors.
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Abstract
Nasopharyngeal carcinoma (NPC) is a cancer that occurs in high frequency in Southern China. A previous functional complementation approach and the subsequent cDNA microarray analysis have identified that serum amyloid A1 (SAA1) is an NPC candidate tumor suppressor gene. SAA1 belongs to a family of acute-phase proteins that are encoded by five polymorphic coding alleles. The SAA1 genotyping results showed that only three SAA1 isoforms (SAA1.1, 1.3 and 1.5) were observed in both Hong Kong NPC patients and healthy individuals. This study aims to determine the functional role of SAA1 polymorphisms in tumor progression and to investigate the relationship between SAA1 polymorphisms and NPC risk. Indeed, we have shown that restoration of SAA1.1 and 1.3 in the SAA1-deficient NPC cell lines could suppress tumor formation and angiogenesis in vitro and in vivo. The secreted SAA1.1 and SAA1.3 proteins can block cell adhesion and induce apoptosis in the vascular endothelial cells. In contrast, the SAA1.5 cannot induce apoptosis or inhibit angiogenesis because of its weaker binding affinity to αVβ3 integrin. This can explain why SAA1.5 has no tumor-suppressive effects. Furthermore, the NPC tumors with this particular SAA1.5/1.5 genotype showed higher levels of SAA1 gene expression, and SAA1.1 and 1.3 alleles were preferentially inactivated in tumor tissues that were examined. These findings further strengthen the conclusion for the defective function of SAA1.5 in suppression of tumor formation and angiogenesis. Interestingly, the frequency of the SAA1.5/1.5 genotype in NPC patients was ~2-fold higher than in the healthy individuals (P=0.00128, odds ratio=2.28), which indicates that this SAA1 genotype is significantly associated with a higher NPC risk. Collectively, this homozygous SAA1.5/1.5 genotype appears to be a recessive susceptibility gene, which has lost the antiangiogenic function, whereas SAA1.1 and SAA1.3 are the dominant alleles of the tumor suppressor phenotype.
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