Human ANXA1 peptide

Circulating antibodies to linear peptides derived annexin A1 (ANXA1) and mucin type-1 (MUC1) have been found to be significantly increased in some types of cancer. The present study was then designed to test whether circulating antibodies to the above two tumor-associated antigens were altered in esophageal cancer. An enzymelinked immunosorbent assay was developed in-house to determine circulating IgG against peptide antigens derived from ANXA1 and MUC1, respectively, in 97 patients with esophageal squamous cell carcinoma (ESCC) and 227 healthy subjects. Student's t-test revealed that patients with ESCC had significantly higher levels of anti-ANXA1 IgG (t=4.02, P=0.0001) and male patients appeared to mainly contribute to the increased levels of anti-ANXA1 IgG in the circulation (t=4.21, P=0.0001). However, circulating levels of anti-MUC1 IgG were not significantly altered in ESCC. The anti-ANXA1 IgG levels were decreased with stages of ESCC, of which patients with stage I ESCC had the highest IgG level among all 4 stages (t=4.84, P=0.0001, compared to control subjects). Pearson analysis showed a significant correlation between anti-ANXA1 IgG levels and stages of ESCC (r=0.21, df=90, P=0.044) but no correlation between anti-MUC1 IgG levels and stages of ESCC (r=0.01, df=90, P=0.899). In conclusion, circulating IgG to ANXA1 may be a potential biomarker for early diagnosis of esophageal cancer.

Background: Annexin A1 (AnxA1) is a protein involved in inflammation resolution that might be altered in obesity-associated type 2 diabetes mellitus (DM), which is a chronic inflammatory disease. The aim of this study was to evaluate AnxA1 serum levels in individuals with and without DM stratified according to the body mass index (BMI), and the dynamic of AnxA1 expression in adipose tissue from humans with obesity and non-obesity. Methods: Serum samples were obtained from 41 patients with DM (lean, overweight and obese) and 40 controls, and adipose tissue samples were obtained from 16 individuals with obesity (with or without DM), and 15 controls. Results: DM patients showed similar AnxA1 serum levels when compared to controls. However, when the individuals were stratified according to BMI, AnxA1 levels were higher in individuals with obesity than lean or overweight, and in overweight compared to lean individuals. Moreover, AnxA1 was correlated positively with IL-6 levels. AnxA1 levels were also positively correlated with BMI, waist circumference and waist-to-hip ratio. Furthermore, higher levels of cleaved AnxA1 were observed in adipose tissue from individuals with obesity, independently of DM status. Conclusions: Enhanced levels of AnxA1 in serum of individuals with obesity suggest an attempt to counter-regulate the systemic inflammation process in this disease. However, the higher levels of cleaved AnxA1 in the adipose tissue of individuals with obesity could compromise its anti-inflammatory and proresolving actions, locally. Considering our data, AnxA1 cleavage in the adipose tissue, despite increased serum levels of this protein, and consequently the failure in inflammation resolution, suggests an important pathophysiological mechanism involved in inflammatory status observed in obesity.