Previous studies have demonstrated that sera from patients with prostate cancer (PCa) contain autoantibodies that react with tumor-associated antigens (TAAs). Autoantibodies to cyclin B1 and fourteen other TAAs were detected by enzyme-linked immunosorbent assay (ELISA) and Western blotting in 464 sera from patients with PCa, benign prostatic hyperplasia (BPH), and other controls. Autoantibodies to cyclin B1 were detected in 31.0% of sera from randomly selected patients with PCa versus 4.8% in sera with BPH. In the further analysis, 31.4% of sera from PCa patients at the early stage contained anti-cyclin B1 autoantibody, and even 29.4% of patients who had normal prostate-specific antigen (PSA) levels in their serum samples were observed anti-cyclin B1 positive. The cumulative positive rate of autoantibodies against seven selected TAAs (cyclin B1, survivin, p53, DFS70/LEDGFp75, RalA, MDM2, and NPM1) in PCa reached 80.5%, significantly higher than that in normal control sera. In summary, autoantibody to cyclin B1 might be a potential biomarker for the immunodiagnosis of early stage PCa, especially useful in patients with normal PSA level. This study further supports the hypothesis that a customized TAA array can be used for enhancing anti-TAA autoantibody detection, and it may constitute a promising and powerful tool for immunodiagnosis of PCa.
HCC1 was originally cloned as a cell nuclear autoantigen in a patient with liver cirrhosis that progressed to HCC. The full-length sequence of HCC1encodes a protein of 530 amino acids and migrating at 64 kDa in SDS-PAGE. HCC1 has two isoforms of HCC1.4 and HCC1.3. The difference is that HCC1.3 has 6-amino acid deletion located in the RNP-1-like region of the putative third RNP-CS domain. The nucleotides and protein sequences of HCC1 were not found at that time in searching available databases and, therefore, it was considered as a novel gene with unknown function. Several years later, a group showed that HCC1 was a co-activator of activating protein-1 and estrogen receptors and proposed naming it CAPER. Further study by other group has demonstrated that HCC1/CAPER is a novel transcriptional co-activator for v-Rel that strongly suppresses its transforming activity, uncovering a tumor suppressor role for HCC1/CAPER in regulating Rel's oncogenic activity. Our previous studies have demonstrated that autoantibodies against tumor-associated antigens (TAAs) can be regarded as serological biomarkers in cancer immunodiagnosis. Whether autoantibodies to HCC1/CAPER can be also used as one of the markers in HCC remains to be investigated. In the present study, autoantibody responses to HCC1.3 and HCC1.4 were firstly evaluated by ELISA, western blotting and indirect immunofluorescence assay in sera from patients with HCC, liver cirrhosis and chronic hepatitis, as well as from normal human individuals. Immunohistochemistry (IHC) with HCC tissue array slides was also performed to analyze protein expression profiles of HCC1. The prevalence of anti-HCC1.4 antibodies was 13.5% (23/171) in HCC, which was significantly higher than that in normal human sera (1.1%). Whereas the significant difference regarding frequency of anti-HCC1.3 antibodies between HCC patients and normal individuals was not found. The frequency of HCC1 expression in HCC tissues was also significantly higher than that in normal liver tissues (57.5% vs. 0%; P<0.001). The data suggests that anti-HCC1.4 autoantibody may be a potential biomarker for HCC, but not HCC1.3. Further functional study of HCC1 may provide more evidence to address the question why these two isoforms of HCC1 can induce different humoral immune response in HCC patients. Citation Format: Liping Dai, Pengfei Ren, Xinxin Liu, Rosalia Ortega, Wu Yao, Kaijuan Wang, Mingan Wang, Eng M. Tan, Jianying Zhang. Humoral autoimmune response to a RNA-binding protein HCC1/CAPER in hepatocellular carcinoma (HCC). [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1256. doi:10.1158/1538-7445.AM2013-1256
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